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Publications of Ahmad Hariri    :chronological  alphabetical  combined listing:

%% Journal Articles   
@article{fds329035,
   Author = {Kim, MJ and Avinun, R and Knodt, AR and Radtke, SR and Hariri,
             AR},
   Title = {Neurogenetic plasticity and sex influence the link between
             corticolimbic structural connectivity and trait
             anxiety},
   Journal = {Scientific Reports},
   Volume = {7},
   Number = {1},
   Year = {2017},
   Month = {December},
   url = {http://dx.doi.org/10.1038/s41598-017-11497-2},
   Doi = {10.1038/s41598-017-11497-2},
   Key = {fds329035}
}

@article{fds329468,
   Author = {Avinun, R and Nevo, A and Knodt, AR and Elliott, ML and Radtke, SR and Brigidi, BD and Hariri, AR},
   Title = {Reward-Related Ventral Striatum Activity Buffers against the
             Experience of Depressive Symptoms Associated with Sleep
             Disturbances.},
   Journal = {The Journal of neuroscience : the official journal of the
             Society for Neuroscience},
   Volume = {37},
   Number = {40},
   Pages = {9724-9729},
   Year = {2017},
   Month = {October},
   url = {http://dx.doi.org/10.1523/jneurosci.1734-17.2017},
   Abstract = {Sleep disturbances represent one risk factor for depression.
             Reward-related brain function, particularly the activity of
             the ventral striatum (VS), has been identified as a
             potential buffer against stress-related depression. We were
             therefore interested in testing whether reward-related VS
             activity would moderate the effect of sleep disturbances on
             depression in a large cohort of young adults. Data were
             available from 1129 university students (mean age 19.71 ±
             1.25 years; 637 women) who completed a reward-related
             functional MRI task to assay VS activity and provided
             self-reports of sleep using the Pittsburgh Sleep Quality
             Index and symptoms of depression using a summation of the
             General Distress/Depression and Anhedonic Depression
             subscales of the Mood and Anxiety Symptoms
             Questionnaire-short form. Analyses revealed that as VS
             activity increased the association between sleep
             disturbances and depressive symptoms decreased. The
             interaction between sleep disturbances and VS activity was
             robust to the inclusion of sex, age, race/ethnicity, past or
             present clinical disorder, early and recent life stress, and
             anxiety symptoms, as well as the interactions between VS
             activity and early or recent life stress as covariates. We
             provide initial evidence that high reward-related VS
             activity may buffer against depressive symptoms associated
             with poor sleep. Our analyses help advance an emerging
             literature supporting the importance of individual
             differences in reward-related brain function as a potential
             biomarker of relative risk for depression.SIGNIFICANCE
             STATEMENT Sleep disturbances are a common risk factor for
             depression. An emerging literature suggests that
             reward-related activity of the ventral striatum (VS), a
             brain region critical for motivation and goal-directed
             behavior, may buffer against the effect of negative
             experiences on the development of depression. Using data
             from a large sample of 1129 university students we
             demonstrate that as reward-related VS activity increases,
             the link between sleep disturbances and depression
             decreases. This finding contributes to accumulating research
             demonstrating that reward-related brain function may be a
             useful biomarker of relative risk for depression in the
             context of negative experiences.},
   Doi = {10.1523/jneurosci.1734-17.2017},
   Key = {fds329468}
}

@article{fds325037,
   Author = {Bogdan, R and Salmeron, BJ and Carey, CE and Agrawal, A and Calhoun, VD and Garavan, H and Hariri, AR and Heinz, A and Hill, MN and Holmes, A and Kalin, NH and Goldman, D},
   Title = {Imaging Genetics and Genomics in Psychiatry: A Critical
             Review of Progress and Potential},
   Journal = {Biological Psychiatry},
   Volume = {82},
   Number = {3},
   Pages = {165-175},
   Year = {2017},
   Month = {August},
   url = {http://dx.doi.org/10.1016/j.biopsych.2016.12.030},
   Doi = {10.1016/j.biopsych.2016.12.030},
   Key = {fds325037}
}

@article{fds315805,
   Author = {Scult, MA and Knodt, AR and Hanson, JL and Ryoo, M and Adcock, RA and Hariri, AR and Strauman, TJ},
   Title = {Individual differences in regulatory focus predict neural
             response to reward.},
   Journal = {Social Neuroscience},
   Volume = {12},
   Number = {4},
   Pages = {419-429},
   Year = {2017},
   Month = {August},
   ISSN = {1747-0919},
   url = {http://dx.doi.org/10.1080/17470919.2016.1178170},
   Abstract = {Although goal pursuit is related to both functioning of the
             brain's reward circuits and psychological factors, the
             literatures surrounding these concepts have often been
             separate. Here, we use the psychological construct of
             regulatory focus to investigate individual differences in
             neural response to reward. Regulatory focus theory proposes
             two motivational orientations for personal goal pursuit: (1)
             promotion, associated with sensitivity to potential gain,
             and (2) prevention, associated with sensitivity to potential
             loss. The monetary incentive delay task was used to
             manipulate reward circuit function, along with instructional
             framing corresponding to promotion and prevention in a
             within-subject design. We observed that the more promotion
             oriented an individual was, the lower their ventral striatum
             response to gain cues. Follow-up analyses revealed that
             greater promotion orientation was associated with decreased
             ventral striatum response even to no-value cues, suggesting
             that promotion orientation may be associated with relatively
             hypoactive reward system function. The findings are also
             likely to represent an interaction between the cognitive and
             motivational characteristics of the promotion system with
             the task demands. Prevention orientation did not correlate
             with ventral striatum response to gain cues, supporting the
             discriminant validity of regulatory focus theory. The
             results highlight a dynamic association between individual
             differences in self-regulation and reward system
             function.},
   Doi = {10.1080/17470919.2016.1178170},
   Key = {fds315805}
}

@article{fds328846,
   Author = {Gard, AM and Waller, R and Shaw, DS and Forbes, EE and Hariri, AR and Hyde,
             LW},
   Title = {The Long Reach of Early Adversity: Parenting, Stress, and
             Neural Pathways to Antisocial Behavior in
             Adulthood},
   Journal = {Biological psychiatry : cognitive neuroscience and
             neuroimaging},
   Year = {2017},
   Month = {June},
   url = {http://dx.doi.org/10.1016/j.bpsc.2017.06.005},
   Doi = {10.1016/j.bpsc.2017.06.005},
   Key = {fds328846}
}

@article{fds325971,
   Author = {Di Iorio and CR and Carey, CE and Michalski, LJ and Corral-Frias, NS and Conley, ED and Hariri, AR and Bogdan, R},
   Title = {Hypothalamic-pituitary-adrenal axis genetic variation and
             early stress moderates amygdala function},
   Journal = {Psychoneuroendocrinology},
   Volume = {80},
   Pages = {170-178},
   Year = {2017},
   Month = {June},
   url = {http://dx.doi.org/10.1016/j.psyneuen.2017.03.016},
   Doi = {10.1016/j.psyneuen.2017.03.016},
   Key = {fds325971}
}

@article{fds326208,
   Author = {Romer, AL and Knodt, AR and Houts, R and Brigidi, BD and Moffitt, TE and Caspi, A and Hariri, AR},
   Title = {Structural alterations within cerebellar circuitry are
             associated with general liability for common mental
             disorders.},
   Journal = {Molecular Psychiatry},
   Year = {2017},
   Month = {April},
   url = {http://dx.doi.org/10.1038/mp.2017.57},
   Abstract = {Accumulating mental-health research encourages a shift in
             focus toward transdiagnostic dimensional features that are
             shared across categorical disorders. In support of this
             shift, recent studies have identified a general liability
             factor for psychopathology-sometimes called the 'p factor'-
             that underlies shared risk for a wide range of mental
             disorders. Identifying neural correlates of this general
             liability would substantiate its importance in
             characterizing the shared origins of mental disorders and
             help us begin to understand the mechanisms through which the
             'p factor' contributes to risk. Here we believe we first
             replicate the 'p factor' using cross-sectional data from a
             volunteer sample of 1246 university students, and then using
             high-resolution multimodal structural neuroimaging, we
             demonstrate that individuals with higher 'p factor' scores
             show reduced structural integrity of white matter pathways,
             as indexed by lower fractional anisotropy values, uniquely
             within the pons. Whole-brain analyses further revealed that
             higher 'p factor' scores are associated with reduced gray
             matter volume in the occipital lobe and left cerebellar
             lobule VIIb, which is functionally connected with prefrontal
             regions supporting cognitive control. Consistent with the
             preponderance of cerebellar afferents within the pons, we
             observed a significant positive correlation between the
             white matter integrity of the pons and cerebellar gray
             matter volume associated with higher 'p factor' scores. The
             results of our analyses provide initial evidence that
             structural alterations in corticocerebellar circuitry
             supporting core functions related to the basic integration,
             coordination and monitoring of information may contribute to
             a general liability for common mental disorders.Molecular
             Psychiatry advance online publication, 11 April 2017;
             doi:10.1038/mp.2017.57.},
   Doi = {10.1038/mp.2017.57},
   Key = {fds326208}
}

@article{fds325036,
   Author = {Dotterer, HL and Hyde, LW and Swartz, JR and Hariri, AR and Williamson,
             DE},
   Title = {Amygdala reactivity predicts adolescent antisocial behavior
             but not callous-unemotional traits},
   Journal = {Developmental Cognitive Neuroscience},
   Volume = {24},
   Pages = {84-92},
   Year = {2017},
   Month = {April},
   url = {http://dx.doi.org/10.1016/j.dcn.2017.02.008},
   Doi = {10.1016/j.dcn.2017.02.008},
   Key = {fds325036}
}

@article{fds325035,
   Author = {Swartz, JR and Prather, AA and Hariri, AR},
   Title = {Threat-related amygdala activity is associated with
             peripheral CRP concentrations in men but not
             women.},
   Journal = {Psychoneuroendocrinology},
   Volume = {78},
   Pages = {93-96},
   Year = {2017},
   Month = {April},
   url = {http://dx.doi.org/10.1016/j.psyneuen.2017.01.024},
   Abstract = {Increased levels of peripheral inflammatory markers,
             including C-Reactive Protein (CRP), are associated with
             increased risk for depression, anxiety, and suicidality. The
             brain mechanisms that may underlie the association between
             peripheral inflammation and internalizing problems remain to
             be determined. The present study examines associations
             between peripheral CRP concentrations and threat-related
             amygdala activity, a neural biomarker of depression and
             anxiety risk, in a sample of 172 young adult undergraduate
             students. Participants underwent functional MRI scanning
             while performing an emotional face matching task to obtain a
             measure of threat-related amygdala activity to angry and
             fearful faces; CRP concentrations were assayed from dried
             blood spots. Results indicated a significant interaction
             between CRP and sex: in men, but not women, higher CRP was
             associated with higher threat-related amygdala activity.
             These results add to the literature finding associations
             between systemic levels of inflammation and brain function
             and suggest that threat-related amygdala activity may serve
             as a potential pathway through which heightened chronic
             inflammation may increase risk for mood and anxiety
             problems.},
   Doi = {10.1016/j.psyneuen.2017.01.024},
   Key = {fds325035}
}

@article{fds323253,
   Author = {Carey, CE and Knodt, AR and Conley, ED and Hariri, AR and Bogdan,
             R},
   Title = {Reward-Related Ventral Striatum Activity Links Polygenic
             Risk for Attention-Deficit/Hyperactivity Disorder to
             Problematic Alcohol Use in Young Adulthood},
   Journal = {Biological psychiatry : cognitive neuroscience and
             neuroimaging},
   Volume = {2},
   Number = {2},
   Pages = {180-187},
   Year = {2017},
   Month = {March},
   url = {http://dx.doi.org/10.1016/j.bpsc.2016.10.003},
   Doi = {10.1016/j.bpsc.2016.10.003},
   Key = {fds323253}
}

@article{fds323689,
   Author = {Trampush, JW and Yang, MLZ and Yu, J and Knowles, E and Davies, G and Liewald, DC and Starr, JM and Djurovic, S and Melle, I and Sundet, K and Christoforou, A and Reinvang, I and DeRosse, P and Lundervold, AJ and Steen, VM and Espeseth, T and Räikkönen, K and Widen, E and Palotie,
             A and Eriksson, JG and Giegling, I and Konte, B and Roussos, P and Giakoumaki, S and Burdick, KE and Payton, A and Ollier, W and Horan, M and Chiba-Falek, O and Attix, DK and Need, AC and Cirulli, ET and Voineskos,
             AN and Stefanis, NC and Avramopoulos, D and Hatzimanolis, A and Arking,
             DE and Smyrnis, N and Bilder, RM et al.},
   Title = {GWAS meta-analysis reveals novel loci and genetic correlates
             for general cognitive function: a report from the COGENT
             consortium.},
   Journal = {Molecular Psychiatry},
   Volume = {22},
   Number = {3},
   Pages = {336-345},
   Year = {2017},
   Month = {March},
   url = {http://dx.doi.org/10.1038/mp.2016.244},
   Abstract = {The complex nature of human cognition has resulted in
             cognitive genomics lagging behind many other fields in terms
             of gene discovery using genome-wide association study (GWAS)
             methods. In an attempt to overcome these barriers, the
             current study utilized GWAS meta-analysis to examine the
             association of common genetic variation (~8M
             single-nucleotide polymorphisms (SNP) with minor allele
             frequency ⩾1%) to general cognitive function in a sample
             of 35 298 healthy individuals of European ancestry across
             24 cohorts in the Cognitive Genomics Consortium (COGENT). In
             addition, we utilized individual SNP lookups and polygenic
             score analyses to identify genetic overlap with other
             relevant neurobehavioral phenotypes. Our primary GWAS
             meta-analysis identified two novel SNP loci (top SNPs:
             rs76114856 in the CENPO gene on chromosome 2 and rs6669072
             near LOC105378853 on chromosome 1) associated with cognitive
             performance at the genome-wide significance level (P<5 ×
             10-8). Gene-based analysis identified an additional three
             Bonferroni-corrected significant loci at chromosomes
             17q21.31, 17p13.1 and 1p13.3. Altogether, common variation
             across the genome resulted in a conservatively estimated SNP
             heritability of 21.5% (s.e.=0.01%) for general cognitive
             function. Integration with prior GWAS of cognitive
             performance and educational attainment yielded several
             additional significant loci. Finally, we found robust
             polygenic correlations between cognitive performance and
             educational attainment, several psychiatric disorders, birth
             length/weight and smoking behavior, as well as a novel
             genetic association to the personality trait of openness.
             These data provide new insight into the genetics of
             neurocognitive function with relevance to understanding the
             pathophysiology of neuropsychiatric illness.},
   Doi = {10.1038/mp.2016.244},
   Key = {fds323689}
}

@article{fds322497,
   Author = {Swartz, JR and Knodt, AR and Radtke, SR and Hariri,
             AR},
   Title = {Peering into the brain to predict behavior: Peer-reported,
             but not self-reported, conscientiousness links
             threat-related amygdala activity to future problem
             drinking.},
   Journal = {NeuroImage},
   Volume = {146},
   Pages = {894-903},
   Year = {2017},
   Month = {February},
   url = {http://dx.doi.org/10.1016/j.neuroimage.2016.10.003},
   Abstract = {Personality traits such as conscientiousness as
             self-reported by individuals can help predict a range of
             outcomes, from job performance to longevity. Asking others
             to rate the personality of their acquaintances often
             provides even better predictive power than using
             self-report. Here, we examine whether peer-reported
             personality can provide a better link between brain
             function, namely threat-related amygdala activity, and
             future health-related behavior, namely problem drinking,
             than self-reported personality. Using data from a sample of
             377 young adult university students who were rated on five
             personality traits by peers, we find that higher
             threat-related amygdala activity to fearful facial
             expressions is associated with higher peer-reported, but not
             self-reported, conscientiousness. Moreover, higher
             peer-reported, but not self-reported, conscientiousness
             predicts lower future problem drinking more than one year
             later, an effect specific to men. Remarkably, relatively
             higher amygdala activity has an indirect effect on future
             drinking behavior in men, linked by peer-reported
             conscientiousness to lower future problem drinking. Our
             results provide initial evidence that the perceived
             conscientiousness of an individual by their peers uniquely
             reflects variability in a core neural mechanism supporting
             threat responsiveness. These novel patterns further suggest
             that incorporating peer-reported measures of personality
             into individual differences research can reveal novel
             predictive pathways of risk and protection for problem
             behaviors.},
   Doi = {10.1016/j.neuroimage.2016.10.003},
   Key = {fds322497}
}

@article{fds316880,
   Author = {Swartz, JR and Hariri, AR and Williamson, DE},
   Title = {An epigenetic mechanism links socioeconomic status to
             changes in depression-related brain function in high-risk
             adolescents.},
   Journal = {Molecular Psychiatry},
   Volume = {22},
   Number = {2},
   Pages = {209-214},
   Year = {2017},
   Month = {February},
   ISSN = {1359-4184},
   url = {http://dx.doi.org/10.1038/mp.2016.82},
   Abstract = {Identifying biological mechanisms through which the
             experience of adversity emerges as individual risk for
             mental illness is an important step toward developing
             strategies for personalized treatment and, ultimately,
             prevention. Preclinical studies have identified epigenetic
             modification of gene expression as one such mechanism.
             Recent clinical studies have suggested that epigenetic
             modification, particularly methylation of gene regulatory
             regions, also acts to shape human brain function associated
             with risk for mental illness. However, it is not yet clear
             whether differential gene methylation as a function of
             adversity contributes to the emergence of individual risk
             for mental illness. Using prospective longitudinal
             epigenetic, neuroimaging and behavioral data from 132
             adolescents, we demonstrate that changes in gene methylation
             associated with lower socioeconomic status (SES) predict
             changes in risk-related brain function. Specifically, we
             find that lower SES during adolescence is associated with an
             increase in methylation of the proximal promoter of the
             serotonin transporter gene, which predicts greater increases
             in threat-related amygdala reactivity. We subsequently
             demonstrate that greater increases in amygdala reactivity
             moderate the association between a positive family history
             for depression and the later manifestation of depressive
             symptoms. These initial results suggest a specific
             biological mechanism through which adversity contributes to
             altered brain function, which in turn moderates the
             emergence of general liability as individual risk for mental
             illness. If replicated, this prospective pathway may
             represent a novel target biomarker for intervention and
             prevention among high-risk individuals.},
   Doi = {10.1038/mp.2016.82},
   Key = {fds316880}
}

@article{fds318715,
   Author = {Swartz, JR and Prather, AA and Di Iorio and CR and Bogdan, R and Hariri,
             AR},
   Title = {A Functional Interleukin-18 Haplotype Predicts Depression
             and Anxiety through Increased Threat-Related Amygdala
             Reactivity in Women but Not Men.},
   Journal = {Neuropsychopharmacology},
   Volume = {42},
   Number = {2},
   Pages = {419-426},
   Year = {2017},
   Month = {January},
   url = {http://dx.doi.org/10.1038/npp.2016.129},
   Abstract = {Common functional polymorphisms in the gene encoding
             interleukin-18 (IL18), a cytokine belonging to the IL-1
             superfamily that can induce synthesis of several other
             cytokines, have been associated with major depressive
             episodes following the experience of stressful life events.
             The neural mechanisms underlying these associations remain
             unexamined. Here we use an imaging genetics strategy to
             examine the effects of risk-related IL18 haplotypes
             comprising rs187238 and rs1946518 on threat-related amygdala
             reactivity and, through an indirect effect, stress-related
             symptoms of depression and anxiety in 448 non-Hispanic
             Caucasian university students. Analyses indicated that women
             but not men possessing an IL18 haplotype comprising both
             risk-related alleles evidenced increased threat-related left
             centromedial amygdala reactivity relative to other haplotype
             groups. Moreover, in women only, increased threat-related
             left centromedial amygdala reactivity predicted increased
             symptoms of depression and anxiety in individuals also
             reporting higher levels of life stress. Path analyses
             revealed a significant indirect effect of IL18 risk
             haplotype on symptoms of depression and anxiety through
             increased threat-related amygdala reactivity. These results
             suggest that a common functional IL18 haplotype associated
             with heightened proinflammatory responses confers
             susceptibility to stress-related depression and anxiety
             through effects on threat-related amygdala function, a risk
             pathway specific to women. If replicated, these patterns can
             inform the search for personalized interventions targeting
             neurobiological pathways of risk associated with
             inflammation.},
   Doi = {10.1038/npp.2016.129},
   Key = {fds318715}
}

@article{fds323776,
   Author = {Scult, MA and Knodt, AR and Swartz, JR and Brigidi, BD and Hariri,
             AR},
   Title = {Thinking and Feeling: Individual Differences in Habitual
             Emotion Regulation and Stress-Related Mood are Associated
             with Prefrontal Executive Control.},
   Journal = {Clinical Psychological Science},
   Volume = {5},
   Number = {1},
   Pages = {150-157},
   Year = {2017},
   Month = {January},
   url = {http://dx.doi.org/10.1177/2167702616654688},
   Abstract = {Calculating math problems from memory may seem unrelated to
             everyday processing of emotions, but they have more in
             common than one might think. Prior research highlights the
             importance of the dorsolateral prefrontal cortex (dlPFC) in
             executive control, intentional emotion regulation, and
             experience of dysfunctional mood and anxiety. While it has
             been hypothesized that emotion regulation may be related to
             'cold' (ie. not emotion-related) executive control, this
             assertion has not been tested. We address this gap by
             providing evidence that greater dlPFC activity during 'cold'
             executive control is associated with increased use of
             cognitive reappraisal to regulate emotions in everyday life.
             We then demonstrate that in the presence of increased life
             stress, increased dlPFC activity is associated with lower
             mood and anxiety symptoms and clinical diagnoses.
             Collectively, our results encourage ongoing efforts to
             understand prefrontal executive control as a possible
             intervention target for improving emotion regulation in mood
             and anxiety disorders.},
   Doi = {10.1177/2167702616654688},
   Key = {fds323776}
}

@article{fds318712,
   Author = {Scult, MA and Paulli, AR and Mazure, ES and Moffitt, TE and Hariri, AR and Strauman, TJ},
   Title = {The association between cognitive function and subsequent
             depression: a systematic review and meta-analysis.},
   Journal = {Psychological Medicine},
   Volume = {47},
   Number = {1},
   Pages = {1-17},
   Year = {2017},
   Month = {January},
   url = {http://dx.doi.org/10.1017/s0033291716002075},
   Abstract = {Despite a growing interest in understanding the cognitive
             deficits associated with major depressive disorder (MDD), it
             is largely unknown whether such deficits exist before
             disorder onset or how they might influence the severity of
             subsequent illness. The purpose of the present study was to
             conduct a systematic review and meta-analysis of
             longitudinal datasets to determine whether cognitive
             function acts as a predictor of later MDD diagnosis or
             change in depression symptoms. Eligible studies included
             longitudinal designs with baseline measures of cognitive
             functioning, and later unipolar MDD diagnosis or symptom
             assessment. The systematic review identified 29
             publications, representing 34 unique samples, and 121 749
             participants, that met the inclusion/exclusion criteria.
             Quantitative meta-analysis demonstrated that higher
             cognitive function was associated with decreased levels of
             subsequent depression (r = -0.088, 95% confidence interval.
             -0.121 to -0.054, p < 0.001). However, sensitivity analyses
             revealed that this association is likely driven by
             concurrent depression symptoms at the time of cognitive
             assessment. Our review and meta-analysis indicate that the
             association between lower cognitive function and later
             depression is confounded by the presence of contemporaneous
             depression symptoms at the time of cognitive assessment.
             Thus, cognitive deficits predicting MDD likely represent
             deleterious effects of subclinical depression symptoms on
             performance rather than premorbid risk factors for
             disorder.},
   Doi = {10.1017/s0033291716002075},
   Key = {fds318712}
}

@article{fds318709,
   Author = {Pornpattananangkul, N and Hariri, AR and Harada, T and Mano, Y and Komeda, H and Parrish, TB and Sadato, N and Iidaka, T and Chiao,
             JY},
   Title = {Cultural influences on neural basis of inhibitory
             control},
   Journal = {NeuroImage},
   Volume = {139},
   Pages = {114-126},
   Year = {2016},
   Month = {October},
   url = {http://dx.doi.org/10.1016/j.neuroimage.2016.05.061},
   Doi = {10.1016/j.neuroimage.2016.05.061},
   Key = {fds318709}
}

@article{fds318711,
   Author = {Kragel, PA and Knodt, AR and Hariri, AR and LaBar,
             KS},
   Title = {Decoding Spontaneous Emotional States in the Human
             Brain.},
   Journal = {PLoS biology},
   Volume = {14},
   Number = {9},
   Pages = {e2000106},
   Year = {2016},
   Month = {September},
   url = {http://dx.doi.org/10.1371/journal.pbio.2000106},
   Abstract = {Pattern classification of human brain activity provides
             unique insight into the neural underpinnings of diverse
             mental states. These multivariate tools have recently been
             used within the field of affective neuroscience to classify
             distributed patterns of brain activation evoked during
             emotion induction procedures. Here we assess whether neural
             models developed to discriminate among distinct emotion
             categories exhibit predictive validity in the absence of
             exteroceptive emotional stimulation. In two experiments, we
             show that spontaneous fluctuations in human resting-state
             brain activity can be decoded into categories of experience
             delineating unique emotional states that exhibit
             spatiotemporal coherence, covary with individual differences
             in mood and personality traits, and predict on-line,
             self-reported feelings. These findings validate objective,
             brain-based models of emotion and show how emotional states
             dynamically emerge from the activity of separable neural
             systems.},
   Doi = {10.1371/journal.pbio.2000106},
   Key = {fds318711}
}

@article{fds318710,
   Author = {Nikolova, YS and Swartz, JR and Hariri, AR},
   Title = {Can we identify meaningful epigenetic effects on human brain
             function and related risk for mental illness?},
   Journal = {Epigenomics},
   Volume = {8},
   Number = {10},
   Pages = {1307-1310},
   Year = {2016},
   Month = {September},
   url = {http://dx.doi.org/10.2217/epi-2016-0099},
   Doi = {10.2217/epi-2016-0099},
   Key = {fds318710}
}

@article{fds318713,
   Author = {Demers, CH and Drabant Conley and E and Bogdan, R and Hariri,
             AR},
   Title = {Interactions Between Anandamide and Corticotropin-Releasing
             Factor Signaling Modulate Human Amygdala Function and Risk
             for Anxiety Disorders: An Imaging Genetics Strategy for
             Modeling Molecular Interactions.},
   Journal = {Biological Psychiatry},
   Volume = {80},
   Number = {5},
   Pages = {356-362},
   Year = {2016},
   Month = {September},
   url = {http://dx.doi.org/10.1016/j.biopsych.2015.12.021},
   Abstract = {Preclinical models reveal that stress-induced amygdala
             activity and impairment in fear extinction reflect
             reductions in anandamide driven by corticotropin-releasing
             factor receptor type 1 (CRF1) potentiation of the anandamide
             catabolic enzyme fatty acid amide hydrolase.Here, we provide
             clinical translation for the importance of these molecular
             interactions using an imaging genetics strategy to examine
             whether interactions between genetic polymorphisms
             associated with differential anandamide (FAAH rs324420) and
             CRF1 (CRHR1 rs110402) signaling modulate amygdala function
             and anxiety disorder diagnosis.Analyses revealed that
             individuals with a genetic background predicting relatively
             high anandamide and CRF1 signaling exhibited blunted
             basolateral amygdala habituation, which further mediated
             increased risk for anxiety disorders among these same
             individuals.The convergence of preclinical and clinical data
             suggests that interactions between anandamide and CRF1
             represent a fundamental molecular mechanism regulating
             amygdala function and anxiety. Our results further highlight
             the potential of imaging genetics to powerfully translate
             complex preclinical findings to clinically meaningful human
             phenotypes.},
   Doi = {10.1016/j.biopsych.2015.12.021},
   Key = {fds318713}
}

@article{fds318714,
   Author = {Waller, R and Corral-Frías, NS and Vannucci, B and Bogdan, R and Knodt,
             AR and Hariri, AR and Hyde, LW},
   Title = {An oxytocin receptor polymorphism predicts amygdala
             reactivity and antisocial behavior in men.},
   Journal = {Social Cognitive and Affective Neuroscience},
   Volume = {11},
   Number = {8},
   Pages = {1218-1226},
   Year = {2016},
   Month = {August},
   url = {http://dx.doi.org/10.1093/scan/nsw042},
   Abstract = {Variability in oxytocin (OXT) signaling is associated with
             individual differences in sex-specific social behavior
             across species. The effects of OXT signaling on social
             behavior are, in part, mediated through its modulation of
             amygdala function. Here, we use imaging genetics to examine
             sex-specific effects of three single-nucleotide
             polymorphisms in the human oxytocin receptor gene (OXTR;
             rs1042778, rs53576 and rs2254298) on threat-related amygdala
             reactivity and social behavior in 406 Caucasians. Analyses
             revealed that among men but not women, OXTR rs1042778 TT
             genotype was associated with increased right amygdala
             reactivity to angry facial expressions, which was uniquely
             related to higher levels of antisocial behavior among men.
             Moderated meditation analysis suggested a trending indirect
             effect of OXTR rs1042778 TT genotype on higher antisocial
             behavior via increased right amygdala reactivity to angry
             facial expressions in men. Our results provide evidence
             linking genetic variation in OXT signaling to individual
             differences in amygdala function. The results further
             suggest that these pathways may be uniquely important in
             shaping antisocial behavior in men.},
   Doi = {10.1093/scan/nsw042},
   Key = {fds318714}
}

@article{fds318716,
   Author = {Krystal, JH and Abi-Dargham, A and Akbarian, S and Arnsten, AFT and Barch, DM and Bearden, CE and Braff, DL and Brown, ES and Bullmore, ET and Carlezon, WA and Carter, CS and Cook, EH and Daskalakis, ZJ and DiLeone,
             RJ and Duman, RS and Grace, AA and Hariri, AR and Harrison, PJ and Hiroi,
             N and Kenny, PJ and Kleinman, JE and Krystal, AD and Lewis, DA and Lipska,
             BK and Marder, SR and Mason, GF and Mathalon, DH and McClung, CA and McDougle, CJ and McIntosh, AM and McMahon, FJ and Mirnics, K and Monteggia, LM and Narendran, R and Nestler, EJ and Neumeister, A and O'Donovan, MC and Öngür, D and Pariante, CM et
             al.},
   Title = {Constance E. Lieber, Theodore R. Stanley, and the Enduring
             Impact of Philanthropy on Psychiatry Research.},
   Journal = {Biological Psychiatry},
   Volume = {80},
   Number = {2},
   Pages = {84-86},
   Year = {2016},
   Month = {July},
   url = {http://dx.doi.org/10.1016/j.biopsych.2016.05.004},
   Doi = {10.1016/j.biopsych.2016.05.004},
   Key = {fds318716}
}

@article{fds316881,
   Author = {Corral-Frías, NS and Pizzagalli, DA and Carré, JM and Michalski,
             LJ and Nikolova, YS and Perlis, RH and Fagerness, J and Lee, MR and Conley,
             ED and Lancaster, TM and Haddad, S and Wolf, A and Smoller, JW and Hariri,
             AR and Bogdan, R},
   Title = {COMT Val(158) Met genotype is associated with reward
             learning: a replication study and meta-analysis.},
   Journal = {Genes, Brain and Behavior},
   Volume = {15},
   Number = {5},
   Pages = {503-513},
   Year = {2016},
   Month = {June},
   ISSN = {1601-1848},
   url = {http://dx.doi.org/10.1111/gbb.12296},
   Abstract = {Identifying mechanisms through which individual differences
             in reward learning emerge offers an opportunity to
             understand both a fundamental form of adaptive responding as
             well as etiological pathways through which aberrant reward
             learning may contribute to maladaptive behaviors and
             psychopathology. One candidate mechanism through which
             individual differences in reward learning may emerge is
             variability in dopaminergic reinforcement signaling. A
             common functional polymorphism within the catechol-O-methyl
             transferase gene (COMT; rs4680, Val(158) Met) has been
             linked to reward learning, where homozygosity for the Met
             allele (linked to heightened prefrontal dopamine function
             and decreased dopamine synthesis in the midbrain) has been
             associated with relatively increased reward learning. Here,
             we used a probabilistic reward learning task to asses
             response bias, a behavioral form of reward learning, across
             three separate samples that were combined for analyses (age:
             21.80 ± 3.95; n = 392; 268 female; European-American: n =
             208). We replicate prior reports that COMT rs4680 Met allele
             homozygosity is associated with increased reward learning in
             European-American participants (β = 0.20, t = 2.75, P <
             0.01; ΔR(2) = 0.04). Moreover, a meta-analysis of 4
             studies, including the current one, confirmed the
             association between COMT rs4680 genotype and reward learning
             (95% CI -0.11 to -0.03; z = 3.2; P < 0.01). These results
             suggest that variability in dopamine signaling associated
             with COMT rs4680 influences individual differences in reward
             which may potentially contribute to psychopathology
             characterized by reward dysfunction.},
   Doi = {10.1111/gbb.12296},
   Key = {fds316881}
}

@article{fds251943,
   Author = {Nelson, EC and Agrawal, A and Heath, AC and Bogdan, R and Sherva, R and Zhang, B and Al-Hasani, R and Bruchas, MR and Chou, Y-L and Demers, CH and Carey, CE and Conley, ED and Fakira, AK and Farrer, LA and Goate, A and Gordon, S and Henders, AK and Hesselbrock, V and Kapoor, M and Lynskey,
             MT and Madden, PAF and Moron, JA and Rice, JP and Saccone, NL and Schwab,
             SG and Shand, FL and Todorov, AA and Wallace, L and Wang, T and Wray, NR and Zhou, X and Degenhardt, L and Martin, NG and Hariri, AR and Kranzler,
             HR and Gelernter, J and Bierut, LJ and Clark, DJ and Montgomery,
             GW},
   Title = {Evidence of CNIH3 involvement in opioid dependence.},
   Journal = {Molecular Psychiatry},
   Volume = {21},
   Number = {5},
   Pages = {608-614},
   Year = {2016},
   Month = {May},
   ISSN = {1359-4184},
   url = {http://dx.doi.org/10.1038/mp.2015.102},
   Abstract = {Opioid dependence, a severe addictive disorder and major
             societal problem, has been demonstrated to be moderately
             heritable. We conducted a genome-wide association study in
             Comorbidity and Trauma Study data comparing opioid-dependent
             daily injectors (N=1167) with opioid misusers who never
             progressed to daily injection (N=161). The strongest
             associations, observed for CNIH3 single-nucleotide
             polymorphisms (SNPs), were confirmed in two independent
             samples, the Yale-Penn genetic studies of opioid, cocaine
             and alcohol dependence and the Study of Addiction: Genetics
             and Environment, which both contain non-dependent opioid
             misusers and opioid-dependent individuals. Meta-analyses
             found five genome-wide significant CNIH3 SNPs. The A allele
             of rs10799590, the most highly associated SNP, was robustly
             protective (P=4.30E-9; odds ratio 0.64 (95% confidence
             interval 0.55-0.74)). Epigenetic annotation predicts that
             this SNP is functional in fetal brain. Neuroimaging data
             from the Duke Neurogenetics Study (N=312) provide evidence
             of this SNP's in vivo functionality; rs10799590 A allele
             carriers displayed significantly greater right amygdala
             habituation to threat-related facial expressions, a
             phenotype associated with resilience to psychopathology.
             Computational genetic analyses of physical dependence on
             morphine across 23 mouse strains yielded significant
             correlations for haplotypes in CNIH3 and functionally
             related genes. These convergent findings support CNIH3
             involvement in the pathophysiology of opioid dependence,
             complementing prior studies implicating the
             α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)
             glutamate system.},
   Doi = {10.1038/mp.2015.102},
   Key = {fds251943}
}

@article{fds313398,
   Author = {Gorka, AX and LaBar, KS and Hariri, AR},
   Title = {Variability in emotional responsiveness and coping style
             during active avoidance as a window onto psychological
             vulnerability to stress.},
   Journal = {Physiology & Behavior},
   Volume = {158},
   Pages = {90-99},
   Year = {2016},
   Month = {May},
   ISSN = {0031-9384},
   url = {http://dx.doi.org/10.1016/j.physbeh.2016.02.036},
   Abstract = {Individual differences in coping styles are associated with
             psychological vulnerability to stress. Recent animal
             research suggests that coping styles reflect trade-offs
             between proactive and reactive threat responses during
             active avoidance paradigms, with proactive responses
             associated with better stress tolerance. Based on these
             preclinical findings, we developed a novel instructed active
             avoidance paradigm to characterize patterns of proactive and
             reactive responses using behavioral, motoric, and autonomic
             measures in humans. Analyses revealed significant
             inter-individual variability not only in the magnitude of
             general emotional responsiveness but also the likelihood to
             specifically express proactive or reactive responses. In men
             but not women, individual differences in general emotional
             responsiveness were linked to increased trait anxiety while
             proactive coping style was linked to increased trait
             aggression. These patterns are consistent with preclinical
             findings and suggest that instructed active avoidance
             paradigms may be useful in assessing psychological
             vulnerability to stress using objective behavioral
             measures.},
   Doi = {10.1016/j.physbeh.2016.02.036},
   Key = {fds313398}
}

@article{fds251941,
   Author = {Nikolova, YS and Knodt, AR and Radtke, SR and Hariri,
             AR},
   Title = {Divergent responses of the amygdala and ventral striatum
             predict stress-related problem drinking in young adults:
             possible differential markers of affective and impulsive
             pathways of risk for alcohol use disorder.},
   Journal = {Molecular Psychiatry},
   Volume = {21},
   Number = {3},
   Pages = {348-356},
   Year = {2016},
   Month = {March},
   ISSN = {1359-4184},
   url = {http://dx.doi.org/10.1038/mp.2015.85},
   Abstract = {Prior work suggests that there may be two distinct pathways
             of alcohol use disorder (AUD) risk: one associated with
             positive emotion enhancement and behavioral impulsivity, and
             another associated with negative emotion relief and coping.
             We sought to map these two pathways onto individual
             differences in neural reward and threat processing assessed
             using blood-oxygen-level-dependent functional magnetic
             resonance imaging in a sample of 759 undergraduate students
             (426 women, mean age 19.65±1.24 years) participating in the
             Duke Neurogenetics Study. We demonstrate that problem
             drinking is highest in the context of stress and in those
             with one of two distinct neural phenotypes: (1) a
             combination of relatively low reward-related activity of the
             ventral striatum (VS) and high threat-related reactivity of
             the amygdala; or (2) a combination of relatively high VS
             activity and low amygdala reactivity. In addition, we
             demonstrate that the relationship between stress and problem
             alcohol use is mediated by impulsivity, as reflected in
             monetary delay discounting rates, for those with high VS-low
             amygdala reactivity, and by anxious/depressive
             symptomatology for those with the opposite neural risk
             phenotype. Across both neural phenotypes, we found that
             greater divergence between VS and amygdala reactivity
             predicted greater risk for problem drinking. Finally, for
             those individuals with the low VS-high amygdala risk
             phenotype we found that stress not only predicted the
             presence of AUD diagnosis at the time of neuroimaging but
             also subsequent problem drinking reported 3 months following
             study completion. These results offer new insight into the
             neural basis of AUD risk and suggest novel biological
             targets for early individualized treatment or
             prevention.},
   Doi = {10.1038/mp.2015.85},
   Key = {fds251941}
}

@article{fds315132,
   Author = {Hanson, JL and Albert, D and Iselin, A-MR and Carré, JM and Dodge, KA and Hariri, AR},
   Title = {Cumulative stress in childhood is associated with blunted
             reward-related brain activity in adulthood.},
   Journal = {Social Cognitive and Affective Neuroscience},
   Volume = {11},
   Number = {3},
   Pages = {405-412},
   Year = {2016},
   Month = {March},
   ISSN = {1749-5016},
   url = {http://hdl.handle.net/10161/10777 Duke open
             access},
   Abstract = {Early life stress (ELS) is strongly associated with negative
             outcomes in adulthood, including reduced motivation and
             increased negative mood. The mechanisms mediating these
             relations, however, are poorly understood. We examined the
             relation between exposure to ELS and reward-related brain
             activity, which is known to predict motivation and mood, at
             age 26, in a sample followed since kindergarten with annual
             assessments. Using functional neuroimaging, we assayed
             individual differences in the activity of the ventral
             striatum (VS) during the processing of monetary rewards
             associated with a simple card-guessing task, in a sample of
             72 male participants. We examined associations between a
             cumulative measure of ELS exposure and VS activity in
             adulthood. We found that greater levels of cumulative stress
             during childhood and adolescence predicted lower
             reward-related VS activity in adulthood. Extending this
             general developmental pattern, we found that exposure to
             stress early in development (between kindergarten and grade
             3) was significantly associated with variability in adult VS
             activity. Our results provide an important demonstration
             that cumulative life stress, especially during this
             childhood period, is associated with blunted reward-related
             VS activity in adulthood. These differences suggest
             neurobiological pathways through which a history of ELS may
             contribute to reduced motivation and increased negative
             mood.},
   Doi = {10.1093/scan/nsv124},
   Key = {fds315132}
}

@article{fds314439,
   Author = {Baranger, DAA and Ifrah, C and Prather, AA and Carey, CE and Corral-Frías, NS and Drabant Conley and E and Hariri, AR and Bogdan,
             R},
   Title = {PER1 rs3027172 Genotype Interacts with Early Life Stress to
             Predict Problematic Alcohol Use, but Not Reward-Related
             Ventral Striatum Activity.},
   Journal = {Frontiers in Psychology},
   Volume = {7},
   Pages = {464},
   Year = {2016},
   Month = {January},
   url = {http://dx.doi.org/10.3389/fpsyg.2016.00464},
   Abstract = {Increasing evidence suggests that the circadian and stress
             regulatory systems contribute to alcohol use disorder (AUD)
             risk, which may partially arise through effects on
             reward-related neural function. The C allele of the PER1
             rs3027172 single nucleotide polymorphism (SNP) reduces PER1
             expression in cells incubated with cortisol and has been
             associated with increased risk for adult AUD and problematic
             drinking among adolescents exposed to high levels of
             familial psychosocial adversity. Using data from
             undergraduate students who completed the ongoing Duke
             Neurogenetics Study (DNS) (n = 665), we tested whether
             exposure to early life stress (ELS; Childhood Trauma
             Questionnaire) moderates the association between rs3027172
             genotype and later problematic alcohol use (Alcohol Use
             Disorders Identification Test) as well as ventral striatum
             (VS) reactivity to reward (card-guessing task while
             functional magnetic resonance imaging data were acquired).
             Initial analyses found that PER1 rs3027172 genotype
             interacted with ELS to predict both problematic drinking and
             VS reactivity; minor C allele carriers, who were also
             exposed to elevated ELS reported greater problematic
             drinking and exhibited greater ventral striatum reactivity
             to reward-related stimuli. When gene × covariate and
             environment × covariate interactions were controlled for,
             the interaction predicting problematic alcohol use remained
             significant (p < 0.05, corrected) while the interaction
             predicting VS reactivity was no longer significant. These
             results extend our understanding of relationships between
             PER1 genotype, ELS, and problematic alcohol use, and serve
             as a cautionary tale on the importance of controlling for
             potential confounders in studies of moderation including
             gene × environment interactions.},
   Doi = {10.3389/fpsyg.2016.00464},
   Key = {fds314439}
}

@article{fds318717,
   Author = {Carey, CE and Agrawal, A and Zhang, B and Conley, ED and Degenhardt, L and Heath, AC and Li, D and Lynskey, MT and Martin, NG and Montgomery, GW and Wang, T and Bierut, LJ and Hariri, AR and Nelson, EC and Bogdan,
             R},
   Title = {Monoacylglycerol lipase (MGLL) polymorphism rs604300
             interacts with childhood adversity to predict cannabis
             dependence symptoms and amygdala habituation: Evidence from
             an endocannabinoid system-level analysis.},
   Journal = {Journal of Abnormal Psychology},
   Volume = {124},
   Number = {4},
   Pages = {860-877},
   Year = {2015},
   Month = {November},
   url = {http://dx.doi.org/10.1037/abn0000079},
   Abstract = {Despite evidence for heritable variation in cannabis
             involvement and the discovery of cannabinoid receptors and
             their endogenous ligands, no consistent patterns have
             emerged from candidate endocannabinoid (eCB) genetic
             association studies of cannabis involvement. Given
             interactions between eCB and stress systems and associations
             between childhood stress and cannabis involvement, it may be
             important to consider childhood adversity in the context of
             eCB-related genetic variation. We employed a system-level
             gene-based analysis of data from the Comorbidity and Trauma
             Study (N = 1,558) to examine whether genetic variation in
             six eCB genes (anabolism: DAGLA, DAGLB, NAPEPLD; catabolism:
             MGLL, FAAH; binding: CNR1; SNPs N = 65) and childhood sexual
             abuse (CSA) predict cannabis dependence symptoms.
             Significant interactions with CSA emerged for MGLL at the
             gene level (p = .009), and for rs604300 within MGLL (ΔR2 =
             .007, p < .001), the latter of which survived SNP-level
             Bonferroni correction and was significant in an additional
             sample with similar directional effects (N = 859; ΔR2 =
             .005, p = .026). Furthermore, in a third sample (N = 312),
             there was evidence that rs604300 genotype interacts with
             early life adversity to predict threat-related basolateral
             amygdala habituation, a neural phenotype linked to the eCB
             system and addiction (ΔR2 = .013, p = .047). Rs604300 may
             be related to epigenetic modulation of MGLL expression.
             These results are consistent with rodent models implicating
             2-arachidonoylglycerol (2-AG), an endogenous cannabinoid
             metabolized by the enzyme encoded by MGLL, in the etiology
             of stress adaptation related to cannabis dependence, but
             require further replication.},
   Doi = {10.1037/abn0000079},
   Key = {fds318717}
}

@article{fds251944,
   Author = {Hanson, JL and Hariri, AR and Williamson, DE},
   Title = {Blunted Ventral Striatum Development in Adolescence Reflects
             Emotional Neglect and Predicts Depressive
             Symptoms.},
   Journal = {Biological Psychiatry},
   Volume = {78},
   Number = {9},
   Pages = {598-605},
   Year = {2015},
   Month = {November},
   ISSN = {0006-3223},
   url = {http://dx.doi.org/10.1016/j.biopsych.2015.05.010},
   Abstract = {Emotional neglect is associated with multiple negative
             outcomes, particularly increased risk for depression.
             Motivated by increasing evidence of reward-related ventral
             striatum (VS) dysfunction in depression, we investigated the
             role of developmental changes in VS activity on the
             emergence of depressive symptomatology as a function of
             emotional neglect.We examined relationships between
             longitudinal neuroimaging of reward-related VS activity,
             assessments of mood, and measures of emotional neglect in
             106 participants first scanned between ages 11 to 15 and
             then 2 years later.We found that greater levels of emotional
             neglect were associated with blunted development of
             reward-related VS activity between the first and second
             assessments (as indexed by lower residualized change
             scores). Additionally, we found that decreases in this
             reward-related VS activity were related to greater
             depressive symptomatology and partially mediated the
             association between emotional neglect and subsequent
             depressive symptomatology.Our results provide an important
             demonstration that blunted development of reward-related VS
             activity as a function of emotional neglect predicts the
             emergence of depressive symptoms in adolescents. Further,
             our results are consistent with emerging evidence for the
             importance of reward-related VS dysfunction in the etiology
             and pathophysiology of depression. These results are a first
             step toward developing the ability to predict, prevent, and
             treat stress-related psychopathology through the targeting
             of specific neural phenotypes.},
   Doi = {10.1016/j.biopsych.2015.05.010},
   Key = {fds251944}
}

@article{fds251937,
   Author = {Hariri, AR and Holmes, A},
   Title = {Finding translation in stress research.},
   Journal = {Nature Neuroscience},
   Volume = {18},
   Number = {10},
   Pages = {1347-1352},
   Year = {2015},
   Month = {October},
   ISSN = {1097-6256},
   url = {http://dx.doi.org/10.1038/nn.4111},
   Abstract = {In our ongoing efforts to advance understanding of human
             diseases, translational research across rodents and humans
             on stress-related mental disorders stands out as a field
             that is producing discoveries that illuminate mechanisms of
             risk and pathophysiology at a brisk rate. Here we offer a
             Perspective on how a productive translational research
             dialog between preclinical models and clinical studies of
             these disorders is being powered by an ever-developing
             appreciation of the shared neural circuits and genetic
             architecture that moderate the response to stress across
             species. Working from these deep foundations, we discuss the
             approaches, both traditional and innovative, that have the
             potential to deliver a new generation of risk biomarkers and
             therapeutic strategies for stress-related
             disorders.},
   Doi = {10.1038/nn.4111},
   Key = {fds251937}
}

@article{fds291135,
   Author = {Scult, MA and Trampush, JW and Zheng, F and Conley, ED and Lencz, T and Malhotra, AK and Dickinson, D and Weinberger, DR and Hariri,
             AR},
   Title = {A Common Polymorphism in SCN2A Predicts General Cognitive
             Ability through Effects on PFC Physiology.},
   Journal = {Journal of Cognitive Neuroscience},
   Volume = {27},
   Number = {9},
   Pages = {1766-1774},
   Year = {2015},
   Month = {September},
   ISSN = {0898-929X},
   url = {http://dx.doi.org/10.1162/jocn_a_00826},
   Abstract = {Here we provide novel convergent evidence across three
             independent cohorts of healthy adults (n = 531),
             demonstrating that a common polymorphism in the gene
             encoding the α2 subunit of neuronal voltage-gated type II
             sodium channels (SCN2A) predicts human general cognitive
             ability or "g." Using meta-analysis, we demonstrate that the
             minor T allele of a common polymorphism (rs10174400) in
             SCN2A is associated with significantly higher "g"
             independent of gender and age. We further demonstrate using
             resting-state fMRI data from our discovery cohort (n = 236)
             that this genetic advantage may be mediated by increased
             capacity for information processing between the dorsolateral
             PFC and dorsal ACC, which support higher cognitive
             functions. Collectively, these findings fill a gap in our
             understanding of the genetics of general cognitive ability
             and highlight a specific neural mechanism through which a
             common polymorphism shapes interindividual variation in
             "g."},
   Doi = {10.1162/jocn_a_00826},
   Key = {fds291135}
}

@article{fds251948,
   Author = {Nikolova, YS and Hariri, AR},
   Title = {Can we observe epigenetic effects on human brain
             function?},
   Journal = {Trends in Cognitive Sciences},
   Volume = {19},
   Number = {7},
   Pages = {366-373},
   Year = {2015},
   Month = {July},
   ISSN = {1364-6613},
   url = {http://dx.doi.org/10.1016/j.tics.2015.05.003},
   Abstract = {Imaging genetics has identified many contributions of DNA
             sequence variation to individual differences in brain
             function, behavior, and risk for psychopathology. Recent
             studies have extended this work beyond the genome by mapping
             epigenetic differences, specifically gene methylation in
             peripherally assessed DNA, onto variability in behaviorally
             and clinically relevant brain function. These data have
             generated understandable enthusiasm for the potential of
             such research to illuminate biological mechanisms of risk.
             We use our research on the effects of genetic and epigenetic
             variation in the human serotonin transporter on brain
             function to generate a guardedly optimistic opinion that the
             available data encourage continued research in this
             direction, and suggest strategies to promote faster
             progress.},
   Doi = {10.1016/j.tics.2015.05.003},
   Key = {fds251948}
}

@article{fds251949,
   Author = {Trampush, JW and Lencz, T and Knowles, E and Davies, G and Guha, S and Pe'er, I and Liewald, DC and Starr, JM and Djurovic, S and Melle, I and Sundet, K and Christoforou, A and Reinvang, I and Mukherjee, S and DeRosse, P and Lundervold, A and Steen, VM and John, M and Espeseth, T and Räikkönen, K and Widen, E and Palotie, A and Eriksson, JG and Giegling, I and Konte, B and Ikeda, M and Roussos, P and Giakoumaki, S and Burdick, KE and Payton, A and Ollier, W and Horan, M and Scult, M and Dickinson, D and Straub, RE and Donohoe, G and Morris, D and Corvin, A and Gill, M and Hariri, A and Weinberger, DR et al.},
   Title = {Independent evidence for an association between general
             cognitive ability and a genetic locus for educational
             attainment.},
   Journal = {American Journal of Medical Genetics Part B:
             Neuropsychiatric Genetics},
   Volume = {168B},
   Number = {5},
   Pages = {363-373},
   Year = {2015},
   Month = {July},
   ISSN = {1552-4841},
   url = {http://dx.doi.org/10.1002/ajmg.b.32319},
   Abstract = {Cognitive deficits and reduced educational achievement are
             common in psychiatric illness; understanding the genetic
             basis of cognitive and educational deficits may be
             informative about the etiology of psychiatric disorders. A
             recent, large genome-wide association study (GWAS) reported
             a genome-wide significant locus for years of education,
             which subsequently demonstrated association to general
             cognitive ability ("g") in overlapping cohorts. The current
             study was designed to test whether GWAS hits for educational
             attainment are involved in general cognitive ability in an
             independent, large-scale collection of cohorts. Using
             cohorts in the Cognitive Genomics Consortium (COGENT; up to
             20,495 healthy individuals), we examined the relationship
             between g and variants associated with educational
             attainment. We next conducted meta-analyses with 24,189
             individuals with neurocognitive data from the educational
             attainment studies, and then with 53,188 largely independent
             individuals from a recent GWAS of cognition. A SNP
             (rs1906252) located at chromosome 6q16.1, previously
             associated with years of schooling, was significantly
             associated with g (P = 1.47 × 10(-4) ) in COGENT.
             The first joint analysis of 43,381 non-overlapping
             individuals for this a priori-designated locus was strongly
             significant (P = 4.94 × 10(-7) ), and the second
             joint analysis of 68,159 non-overlapping individuals was
             even more robust (P = 1.65 × 10(-9) ). These
             results provide independent replication, in a large-scale
             dataset, of a genetic locus associated with cognitive
             function and education. As sample sizes grow, cognitive GWAS
             will identify increasing numbers of associated loci, as has
             been accomplished in other polygenic quantitative traits,
             which may be relevant to psychiatric illness.},
   Doi = {10.1002/ajmg.b.32319},
   Key = {fds251949}
}

@article{fds251938,
   Author = {Telch, MJ and Beevers, CG and Rosenfield, D and Lee, H-J and Reijntjes,
             A and Ferrell, RE and Hariri, AR},
   Title = {5-HTTLPR genotype potentiates the effects of war zone
             stressors on the emergence of PTSD, depressive and anxiety
             symptoms in soldiers deployed to iraq.},
   Journal = {World psychiatry : official journal of the World Psychiatric
             Association (WPA)},
   Volume = {14},
   Number = {2},
   Pages = {198-206},
   Year = {2015},
   Month = {June},
   ISSN = {1723-8617},
   url = {http://dx.doi.org/10.1002/wps.20215},
   Abstract = {Exposure to war zone stressors is common, yet only a
             minority of soldiers experience clinically meaningful
             disturbance in psychological function. Identification of
             biomarkers that predict vulnerability to war zone stressors
             is critical for developing more effective treatment and
             prevention strategies not only in soldiers but also in
             civilians who are exposed to trauma. We investigated the
             role of the serotonin transporter linked polymorphic region
             (5-HTTLPR) genotype in predicting the emergence of
             post-traumatic stress disorder (PTSD), depressive and
             anxiety symptoms as a function of war zone stressors. A
             prospective cohort of 133 U.S. Army soldiers with no prior
             history of deployment to a war zone, who were scheduled to
             deploy to Iraq, was recruited. Multilevel regression models
             were used to investigate associations between 5-HTTLPR
             genotype, level of war zone stressors, and reported symptoms
             of PTSD, depression and anxiety while deployed to Iraq.
             Level of war zone stressors was associated with symptoms of
             PTSD, depression and anxiety. Consistent with its effects on
             stress responsiveness, 5-HTTLPR genotype moderated the
             relationship between level of war zone stressors and
             symptoms of emotional disturbance. Specifically, soldiers
             carrying one or two low functioning alleles (S or LG )
             reported heightened symptoms of PTSD, depression and anxiety
             in response to increased levels of exposure to war zone
             stressors, relative to soldiers homozygous for the high
             functioning allele (LA ). These data suggest that 5-HTTLPR
             genotype moderates individual sensitivity to war zone
             stressors and the expression of emotional disturbance
             including PTSD symptoms. Replication of this association
             along with identification of other genetic moderators of
             risk can inform the development of biomarkers that can
             predict relative resilience vs. vulnerability to
             stress.},
   Doi = {10.1002/wps.20215},
   Key = {fds251938}
}

@article{fds251939,
   Author = {Arloth, J and Bogdan, R and Weber, P and Frishman, G and Menke, A and Wagner, KV and Balsevich, G and Schmidt, MV and Karbalai, N and Czamara,
             D and Altmann, A and Trümbach, D and Wurst, W and Mehta, D and Uhr, M and Klengel, T and Erhardt, A and Carey, CE and Conley, ED and Major
             Depressive Disorder Working Group of the Psychiatric
             Genomics Consortium (PGC), and Ruepp, A and Müller-Myhsok, B and Hariri, AR and Binder, EB and Major Depressive Disorder Working
             Group of the Psychiatric Genomics Consortium
             PGC},
   Title = {Genetic Differences in the Immediate Transcriptome Response
             to Stress Predict Risk-Related Brain Function and
             Psychiatric Disorders.},
   Journal = {Neuron},
   Volume = {86},
   Number = {5},
   Pages = {1189-1202},
   Year = {2015},
   Month = {June},
   ISSN = {0896-6273},
   url = {http://dx.doi.org/10.1016/j.neuron.2015.05.034},
   Abstract = {Depression risk is exacerbated by genetic factors and stress
             exposure; however, the biological mechanisms through which
             these factors interact to confer depression risk are poorly
             understood. One putative biological mechanism implicates
             variability in the ability of cortisol, released in response
             to stress, to trigger a cascade of adaptive genomic and
             non-genomic processes through glucocorticoid receptor (GR)
             activation. Here, we demonstrate that common genetic
             variants in long-range enhancer elements modulate the
             immediate transcriptional response to GR activation in human
             blood cells. These functional genetic variants increase risk
             for depression and co-heritable psychiatric disorders.
             Moreover, these risk variants are associated with
             inappropriate amygdala reactivity, a transdiagnostic
             psychiatric endophenotype and an important stress hormone
             response trigger. Network modeling and animal experiments
             suggest that these genetic differences in GR-induced
             transcriptional activation may mediate the risk for
             depression and other psychiatric disorders by altering a
             network of functionally related stress-sensitive genes in
             blood and brain.},
   Doi = {10.1016/j.neuron.2015.05.034},
   Key = {fds251939}
}

@article{fds251940,
   Author = {Victor, EC and Sansosti, AA and Bowman, HC and Hariri,
             AR},
   Title = {Differential patterns of amygdala and ventral striatum
             activation predict gender-specific changes in sexual risk
             behavior.},
   Journal = {The Journal of neuroscience : the official journal of the
             Society for Neuroscience},
   Volume = {35},
   Number = {23},
   Pages = {8896-8900},
   Year = {2015},
   Month = {June},
   ISSN = {0270-6474},
   url = {http://dx.doi.org/10.1523/jneurosci.0737-15.2015},
   Abstract = {Although the initiation of sexual behavior is common among
             adolescents and young adults, some individuals express this
             behavior in a manner that significantly increases their risk
             for negative outcomes including sexually transmitted
             infections. Based on accumulating evidence, we have
             hypothesized that increased sexual risk behavior reflects,
             in part, an imbalance between neural circuits mediating
             approach and avoidance in particular as manifest by
             relatively increased ventral striatum (VS) activity and
             relatively decreased amygdala activity. Here, we test our
             hypothesis using data from seventy 18- to 22-year-old
             university students participating in the Duke Neurogenetics
             Study. We found a significant three-way interaction between
             amygdala activation, VS activation, and gender predicting
             changes in the number of sexual partners over time. Although
             relatively increased VS activation predicted greater
             increases in sexual partners for both men and women, the
             effect in men was contingent on the presence of relatively
             decreased amygdala activation and the effect in women was
             contingent on the presence of relatively increased amygdala
             activation. These findings suggest unique gender differences
             in how complex interactions between neural circuit function
             contributing to approach and avoidance may be expressed as
             sexual risk behavior in young adults. As such, our findings
             have the potential to inform the development of novel,
             gender-specific strategies that may be more effective at
             curtailing sexual risk behavior.},
   Doi = {10.1523/jneurosci.0737-15.2015},
   Key = {fds251940}
}

@article{fds251946,
   Author = {Gorka, AX and Norman, RE and Radtke, SR and Carré, JM and Hariri,
             AR},
   Title = {Anterior cingulate cortex gray matter volume mediates an
             association between 2D:4D ratio and trait aggression in
             women but not men.},
   Journal = {Psychoneuroendocrinology},
   Volume = {56},
   Pages = {148-156},
   Year = {2015},
   Month = {June},
   ISSN = {0306-4530},
   url = {http://dx.doi.org/10.1016/j.psyneuen.2015.03.004},
   Abstract = {Previous research demonstrates that prenatal testosterone
             exposure increases aggression, possibly through its effects
             on the structure and function of neural circuits supporting
             threat detection and emotion regulation. Here we examined
             associations between regional gray matter volume, trait
             aggression, and the ratio of the second and fourth digit of
             the hand (2D:4D ratio) as a putative index of prenatal
             testosterone exposure in 464 healthy young adult volunteers.
             Our analyses revealed a significant positive correlation
             between 2D:4D ratio and gray matter volume of the dorsal
             anterior cingulate cortex (dACC), a brain region supporting
             emotion regulation, conflict monitoring, and behavioral
             inhibition. Subsequent analyses demonstrated that reduced
             (i.e., masculinized) gray matter volume in the dACC mediated
             the relationship between 2D:4D ratio and aggression in
             women, but not men. Expanding on this gender-specific
             mediation, additional analyses demonstrated that the shared
             variance between 2D:4D ratio, dACC gray matter volume, and
             aggression in women reflected the tendency to engage in
             cognitive reappraisal of emotionally provocative stimuli.
             Our results provide novel evidence that 2D:4D ratio is
             associated with masculinization of dACC gray matter volume,
             and that this neural phenotype mediates, in part, the
             expression of trait aggression in women.},
   Doi = {10.1016/j.psyneuen.2015.03.004},
   Key = {fds251946}
}

@article{fds251953,
   Author = {Kochunov, P and Jahanshad, N and Marcus, D and Winkler, A and Sprooten,
             E and Nichols, TE and Wright, SN and Hong, LE and Patel, B and Behrens, T and Jbabdi, S and Andersson, J and Lenglet, C and Yacoub, E and Moeller, S and Auerbach, E and Ugurbil, K and Sotiropoulos, SN and Brouwer, RM and Landman, B and Lemaitre, H and den Braber, A and Zwiers, MP and Ritchie,
             S and van Hulzen, K and Almasy, L and Curran, J and deZubicaray, GI and Duggirala, R and Fox, P and Martin, NG and McMahon, KL and Mitchell, B and Olvera, RL and Peterson, C and Starr, J and Sussmann, J and Wardlaw, J and Wright, M and Boomsma, DI et al.},
   Title = {Heritability of fractional anisotropy in human white matter:
             a comparison of Human Connectome Project and ENIGMA-DTI
             data.},
   Journal = {NeuroImage},
   Volume = {111},
   Pages = {300-311},
   Year = {2015},
   Month = {May},
   ISSN = {1053-8119},
   url = {http://dx.doi.org/10.1016/j.neuroimage.2015.02.050},
   Abstract = {The degree to which genetic factors influence brain
             connectivity is beginning to be understood. Large-scale
             efforts are underway to map the profile of genetic effects
             in various brain regions. The NIH-funded Human Connectome
             Project (HCP) is providing data valuable for analyzing the
             degree of genetic influence underlying brain connectivity
             revealed by state-of-the-art neuroimaging methods. We
             calculated the heritability of the fractional anisotropy
             (FA) measure derived from diffusion tensor imaging (DTI)
             reconstruction in 481 HCP subjects (194/287 M/F) consisting
             of 57/60 pairs of mono- and dizygotic twins, and 246
             siblings. FA measurements were derived using (Enhancing
             NeuroImaging Genetics through Meta-Analysis) ENIGMA DTI
             protocols and heritability estimates were calculated using
             the SOLAR-Eclipse imaging genetic analysis package. We
             compared heritability estimates derived from HCP data to
             those publicly available through the ENIGMA-DTI consortium,
             which were pooled together from five-family based studies
             across the US, Europe, and Australia. FA measurements from
             the HCP cohort for eleven major white matter tracts were
             highly heritable (h(2)=0.53-0.90, p<10(-5)), and were
             significantly correlated with the joint-analytical estimates
             from the ENIGMA cohort on the tract and voxel-wise levels.
             The similarity in regional heritability suggests that the
             additive genetic contribution to white matter microstructure
             is consistent across populations and imaging acquisition
             parameters. It also suggests that the overarching genetic
             influence provides an opportunity to define a common genetic
             search space for future gene-discovery studies. Uniquely,
             the measurements of additive genetic contribution performed
             in this study can be repeated using online genetic analysis
             tools provided by the HCP ConnectomeDB web
             application.},
   Doi = {10.1016/j.neuroimage.2015.02.050},
   Key = {fds251953}
}

@article{fds251950,
   Author = {Gorka, AX and Knodt, AR and Hariri, AR},
   Title = {Basal forebrain moderates the magnitude of task-dependent
             amygdala functional connectivity.},
   Journal = {Social Cognitive and Affective Neuroscience},
   Volume = {10},
   Number = {4},
   Pages = {501-507},
   Year = {2015},
   Month = {April},
   ISSN = {1749-5016},
   url = {http://dx.doi.org/10.1093/scan/nsu080},
   Abstract = {Animal studies reveal that the amygdala promotes attention
             and emotional memory, in part, by driving activity in
             downstream target regions including the prefrontal cortex
             (PFC) and hippocampus. Prior work has demonstrated that the
             amygdala influences these regions directly through
             monosynaptic glutamatergic signaling, and indirectly by
             driving activity of the cholinergic basal forebrain and
             subsequent downstream acetylcholine release. Yet to date, no
             work has addressed the functional relevance of the
             cholinergic basal forebrain in facilitating signaling from
             the amygdala in humans. We set out to determine how blood
             oxygen level-dependent signal within the amygdala and
             cholinergic basal forebrain interact to predict neural
             responses within downstream targets. Here, we use functional
             connectivity analyses to demonstrate that the cholinergic
             basal forebrain moderates increased amygdala connectivity
             with both the PFC and the hippocampus during the processing
             of biologically salient stimuli in humans. We further
             demonstrate that functional variation within the choline
             transporter gene predicts the magnitude of this modulatory
             effect. Collectively, our results provide novel evidence for
             the importance of cholinergic signaling in modulating neural
             pathways supporting arousal, attention and memory in humans.
             Further, our results may shed light on prior association
             studies linking functional variation within the choline
             transporter gene and diagnoses of major depression and
             attention-deficit hyperactivity disorder.},
   Doi = {10.1093/scan/nsu080},
   Key = {fds251950}
}

@article{fds251952,
   Author = {Swartz, JR and Williamson, DE and Hariri, AR},
   Title = {Developmental change in amygdala reactivity during
             adolescence: effects of family history of depression and
             stressful life events.},
   Journal = {American Journal of Psychiatry},
   Volume = {172},
   Number = {3},
   Pages = {276-283},
   Year = {2015},
   Month = {March},
   ISSN = {0002-953X},
   url = {http://dx.doi.org/10.1176/appi.ajp.2014.14020195},
   Abstract = {Although heightened amygdala reactivity is observed in
             patients with major depression, two critical gaps in our
             knowledge remain. First, it is unclear whether heightened
             amygdala reactivity is a premorbid vulnerability or a
             consequence of the disorder. Second, it is unknown how and
             when this neural phenotype develops. The authors sought to
             address these gaps by evaluating developmental change in
             threat-related amygdala reactivity in adolescents at high or
             low risk for depression based on family history, before
             onset of disorder.At baseline and again 2 years later,
             adolescents (initially 11-15 years of age) participated in a
             functional MRI paradigm that elicited threat-related
             amygdala reactivity. After quality control, data were
             available for 232 adolescents at wave 1 and 197 adolescents
             at wave 2; longitudinal data meeting quality control at both
             waves were available for 157 of these participants. Change
             in amygdala reactivity was assessed as a function of family
             history of depression and severity of stressful life
             events.Threat-related amygdala reactivity increased with age
             in participants with a positive family history regardless of
             the severity of life stress reported, and it increased in
             adolescents with a negative family history who reported
             relatively severe life stress. These changes in amygdala
             reactivity with age occurred in the absence of clinical
             disorder or increases in depressive symptoms.These results
             suggest that heightened amygdala reactivity emerges during
             adolescence, prior to the development of depression, as a
             function of familial risk or, in the absence of familial
             risk, stressful life events.},
   Doi = {10.1176/appi.ajp.2014.14020195},
   Key = {fds251952}
}

@article{fds251955,
   Author = {Swartz, JR and Knodt, AR and Radtke, SR and Hariri,
             AR},
   Title = {A neural biomarker of psychological vulnerability to future
             life stress.},
   Journal = {Neuron},
   Volume = {85},
   Number = {3},
   Pages = {505-511},
   Year = {2015},
   Month = {February},
   ISSN = {0896-6273},
   url = {http://hdl.handle.net/10161/9483 Duke open
             access},
   Abstract = {We all experience a host of common life stressors such as
             the death of a family member, medical illness, and financial
             uncertainty. While most of us are resilient to such
             stressors, continuing to function normally, for a subset of
             individuals, experiencing these stressors increases the
             likelihood of developing treatment-resistant, chronic
             psychological problems, including depression and anxiety. It
             is thus paramount to identify predictive markers of risk,
             particularly those reflecting fundamental biological
             processes that can be targets for intervention and
             prevention. Using data from a longitudinal study of 340
             healthy young adults, we demonstrate that individual
             differences in threat-related amygdala reactivity predict
             psychological vulnerability to life stress occurring as much
             as 1 to 4 years later. These results highlight a readily
             assayed biomarker, threat-related amygdala reactivity, which
             predicts psychological vulnerability to commonly experienced
             stressors and represents a discrete target for intervention
             and prevention.},
   Doi = {10.1016/j.neuron.2014.12.055},
   Key = {fds251955}
}

@article{fds251951,
   Author = {Corral-Frías, NS and Nikolova, YS and Michalski, LJ and Baranger,
             DAA and Hariri, AR and Bogdan, R},
   Title = {Stress-related anhedonia is associated with ventral striatum
             reactivity to reward and transdiagnostic psychiatric
             symptomatology.},
   Journal = {Psychological Medicine},
   Volume = {45},
   Number = {12},
   Pages = {2605-2617},
   Year = {2015},
   Month = {January},
   ISSN = {0033-2917},
   url = {http://dx.doi.org/10.1017/s0033291715000525},
   Abstract = {Early life stress (ELS) is consistently associated with
             increased risk for subsequent psychopathology. Individual
             differences in neural response to reward may confer
             vulnerability to stress-related psychopathology. Using data
             from the ongoing Duke Neurogenetics Study, the present study
             examined whether reward-related ventral striatum (VS)
             reactivity moderates the relationship between
             retrospectively reported ELS and anhedonic symptomatology.
             We further assessed whether individual differences in
             reward-related VS reactivity were associated with other
             depressive symptoms and problematic alcohol use via
             stress-related anhedonic symptoms and substance
             use-associated coping.Blood oxygen level-dependent
             functional magnetic resonance imaging (fMRI) was collected
             while participants (n = 906) completed a card-guessing task,
             which robustly elicits VS reactivity. ELS, anhedonic
             symptoms, other depressive symptoms, coping behavior, and
             alcohol use behavior were assessed with self-report
             questionnaires. Linear regressions were run to examine
             whether VS reactivity moderated the relationship between ELS
             and anhedonic symptoms. Structural equation models examined
             whether this moderation was indirectly associated with other
             depression symptoms and problematic alcohol use through its
             association with anhedonia.Analyses of data from 820
             participants passing quality control procedures revealed
             that the VS × ELS interaction was associated with anhedonic
             symptoms (p = 0.011). Moreover, structural equation models
             indirectly linked this interaction to non-anhedonic
             depression symptoms and problematic alcohol use through
             anhedonic symptoms and substance-related coping.These
             findings suggest that reduced VS reactivity to reward is
             associated with increased risk for anhedonia in individuals
             exposed to ELS. Such stress-related anhedonia is further
             associated with other depressive symptoms and problematic
             alcohol use through substance-related coping.},
   Doi = {10.1017/s0033291715000525},
   Key = {fds251951}
}

@article{fds251954,
   Author = {Carré, JM and Baird-Rowe, CD and Hariri, AR},
   Title = {Testosterone responses to competition predict decreased
             trust ratings of emotionally neutral faces.},
   Journal = {Psychoneuroendocrinology},
   Volume = {49},
   Pages = {79-83},
   Year = {2014},
   Month = {November},
   ISSN = {0306-4530},
   url = {http://dx.doi.org/10.1016/j.psyneuen.2014.06.011},
   Abstract = {A wealth of evidence has linked individual differences in
             testosterone (T) to social, cognitive, and behavioral
             processes related to human dominance. Moreover, recent
             evidence indicates that a single administration of T reduces
             interpersonal trust in healthy young women. Here, in a
             sample of men and women (n=96), we investigated the extent
             to which endogenous fluctuations in T during a competitive
             interaction would predict subsequent ratings of trust from
             emotionally neutral faces. Results indicated that a rise in
             T predicted a decrease in trust ratings in men, but not
             women. These findings provide further support for the idea
             that competition-induced fluctuations in T may serve to
             modulate ongoing and/or future social behavior.},
   Doi = {10.1016/j.psyneuen.2014.06.011},
   Key = {fds251954}
}

@article{Ahs2013,
   Author = {Ahs, F and Davis, CF and Gorka, AX and Hariri, AR},
   Title = {Feature-based representations of emotional facial
             expressions in the human amygdala.},
   Journal = {Social Cognitive and Affective Neuroscience},
   Volume = {9},
   Number = {9},
   Pages = {1372-1378},
   Address = {Center for Cognitive Neuroscience, Duke University Box
             90999, Durham, NC 27708, USA. fredrik.ahs@duke.edu.},
   Year = {2014},
   Month = {September},
   ISSN = {1749-5016},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/23887817},
   Abstract = {The amygdala plays a central role in processing facial
             affect, responding to diverse expressions and features
             shared between expressions. Although speculation exists
             regarding the nature of relationships between expression-
             and feature-specific amygdala reactivity, this matter has
             not been fully explored. We used functional magnetic
             resonance imaging and principal component analysis (PCA) in
             a sample of 300 young adults, to investigate patterns
             related to expression- and feature-specific amygdala
             reactivity to faces displaying neutral, fearful, angry or
             surprised expressions. The PCA revealed a two-dimensional
             correlation structure that distinguished emotional
             categories. The first principal component separated neutral
             and surprised from fearful and angry expressions, whereas
             the second principal component separated neutral and angry
             from fearful and surprised expressions. This two-dimensional
             correlation structure of amygdala reactivity may represent
             specific feature-based cues conserved across discrete
             expressions. To delineate which feature-based cues
             characterized this pattern, face stimuli were averaged and
             then subtracted according to their principal component
             loadings. The first principal component corresponded to
             displacement of the eyebrows, whereas the second principal
             component corresponded to increased exposure of eye whites
             together with movement of the brow. Our results suggest a
             convergent representation of facial affect in the amygdala
             reflecting feature-based processing of discrete
             expressions.},
   Language = {Eng},
   Doi = {10.1093/scan/nst112},
   Key = {Ahs2013}
}

@article{fds251958,
   Author = {Nikolova, YS and Koenen, KC and Galea, S and Wang, C-M and Seney, ML and Sibille, E and Williamson, DE and Hariri, AR},
   Title = {Beyond genotype: serotonin transporter epigenetic
             modification predicts human brain function.},
   Journal = {Nature Neuroscience},
   Volume = {17},
   Number = {9},
   Pages = {1153-1155},
   Year = {2014},
   Month = {September},
   ISSN = {1097-6256},
   url = {http://dx.doi.org/10.1038/nn.3778},
   Abstract = {We examined epigenetic regulation in regards to behaviorally
             and clinically relevant human brain function. Specifically,
             we found that increased promoter methylation of the
             serotonin transporter gene predicted increased
             threat-related amygdala reactivity and decreased mRNA
             expression in postmortem amygdala tissue. These patterns
             were independent of functional genetic variation in the same
             region. Furthermore, the association with amygdala
             reactivity was replicated in a second cohort and was robust
             to both sampling methods and age.},
   Doi = {10.1038/nn.3778},
   Key = {fds251958}
}

@article{fds251956,
   Author = {Bergman, O and Åhs, F and Furmark, T and Appel, L and Linnman, C and Faria, V and Bani, M and Pich, EM and Bettica, P and Henningsson, S and Manuck, SB and Ferrell, RE and Nikolova, YS and Hariri, AR and Fredrikson, M and Westberg, L and Eriksson, E},
   Title = {Association between amygdala reactivity and a dopamine
             transporter gene polymorphism.},
   Journal = {Translational Psychiatry},
   Volume = {4},
   Pages = {e420},
   Year = {2014},
   Month = {August},
   url = {http://dx.doi.org/10.1038/tp.2014.50},
   Abstract = {Essential for detection of relevant external stimuli and for
             fear processing, the amygdala is under modulatory influence
             of dopamine (DA). The DA transporter (DAT) is of fundamental
             importance for the regulation of DA transmission by
             mediating reuptake inactivation of extracellular DA. This
             study examined if a common functional variable number tandem
             repeat polymorphism in the 3' untranslated region of the DAT
             gene (SLC6A3) influences amygdala function during the
             processing of aversive emotional stimuli. Amygdala
             reactivity was examined by comparing regional cerebral blood
             flow, measured with positron emission tomography and
             [(15)O]water, during exposure to angry and neutral faces,
             respectively, in a Swedish sample comprising 32 patients
             with social anxiety disorder and 17 healthy volunteers. In a
             separate US sample, comprising 85 healthy volunteers studied
             with blood oxygen level-dependent functional magnetic
             resonance imaging, amygdala reactivity was assessed by
             comparing the activity during exposure to threatening faces
             and neutral geometric shapes, respectively. In both the
             Swedish and the US sample, 9-repeat carriers displayed
             higher amygdala reactivity than 10-repeat homozygotes. The
             results suggest that this polymorphism contributes to
             individual variability in amygdala reactivity.},
   Doi = {10.1038/tp.2014.50},
   Key = {fds251956}
}

@article{fds251957,
   Author = {Goetz, SMM and Tang, L and Thomason, ME and Diamond, MP and Hariri, AR and Carré, JM},
   Title = {Testosterone rapidly increases neural reactivity to threat
             in healthy men: a novel two-step pharmacological challenge
             paradigm.},
   Journal = {Biological Psychiatry},
   Volume = {76},
   Number = {4},
   Pages = {324-331},
   Year = {2014},
   Month = {August},
   ISSN = {0006-3223},
   url = {http://dx.doi.org/10.1016/j.biopsych.2014.01.016},
   Abstract = {BACKGROUND: Previous research suggests that testosterone (T)
             plays a key role in shaping competitive and aggressive
             behavior in humans, possibly by modulating threat-related
             neural circuitry. However, this research has been limited by
             the use of T augmentation that fails to account for baseline
             differences and has been conducted exclusively in women.
             Thus, the extent to which normal physiologic concentrations
             of T affect threat-related brain function in men remains
             unknown. METHODS: In the current study, we use a novel
             two-step pharmacologic challenge protocol to overcome these
             limitations and to evaluate causal modulation of threat- and
             aggression-related neural circuits by T in healthy young men
             (n = 16). First, we controlled for baseline differences in T
             through administration of a gonadotropin releasing hormone
             antagonist. Once a common baseline was established across
             participants, we then administered T to within the normal
             physiologic range. During this second step of the protocol
             we acquired functional neuroimaging data to examine the
             impact of T augmentation on neural circuitry supporting
             threat and aggression. RESULTS: Gonadotropin releasing
             hormone antagonism successfully reduced circulating
             concentrations of T and brought subjects to a common
             baseline. Administration of T rapidly increased circulating
             T concentrations and was associated with heightened
             reactivity of the amygdala, hypothalamus, and periaqueductal
             grey to angry facial expressions. CONCLUSIONS: These
             findings provide novel causal evidence that T rapidly
             potentiates the response of neural circuits mediating threat
             processing and aggressive behavior in men.},
   Doi = {10.1016/j.biopsych.2014.01.016},
   Key = {fds251957}
}

@article{fds251964,
   Author = {Goetz, SMM and Tang, L and Thomason, ME and Diamond, MP and Hariri, AR and Carré, JM},
   Title = {Testosterone Rapidly Increases Neural Reactivity to Threat
             in Healthy Men: A Novel Two-Step Pharmacological Challenge
             Paradigm},
   Journal = {Biological Psychiatry},
   Volume = {76},
   Number = {4},
   Pages = {324-331},
   Year = {2014},
   Month = {August},
   ISSN = {0006-3223},
   url = {http://dx.doi.org/10.1016/j.biopsych.2014.01.016},
   Doi = {10.1016/j.biopsych.2014.01.016},
   Key = {fds251964}
}

@article{fds251959,
   Author = {Carré, JM and Iselin, A-MR and Welker, KM and Hariri, AR and Dodge,
             KA},
   Title = {Testosterone reactivity to provocation mediates the effect
             of early intervention on aggressive behavior.},
   Journal = {Psychological Science},
   Volume = {25},
   Number = {5},
   Pages = {1140-1146},
   Year = {2014},
   Month = {May},
   ISSN = {0956-7976},
   url = {http://dx.doi.org/10.1177/0956797614525642},
   Abstract = {We tested the hypotheses that the Fast Track intervention
             program for high-risk children would reduce adult aggressive
             behavior and that this effect would be mediated by decreased
             testosterone responses to social provocation. Participants
             were a subsample of males from the full trial sample, who
             during kindergarten had been randomly assigned to the
             10-year Fast Track intervention or to a control group. The
             Fast Track program attempted to develop children's social
             competencies through child social-cognitive and
             emotional-coping skills training, peer-relations coaching,
             academic tutoring, and classroom management, as well as
             training for parents to manage their child's behavior. At a
             mean age of 26 years, participants responded to laboratory
             provocations. Results indicated that, relative to control
             participants, men assigned to the intervention demonstrated
             reduced aggression and testosterone reactivity to social
             provocations. Moreover, reduced testosterone reactivity
             mediated the effect of intervention on aggressive behavior,
             which provides evidence for an enduring biological mechanism
             underlying the effect of early psychosocial intervention on
             aggressive behavior in adulthood.},
   Doi = {10.1177/0956797614525642},
   Key = {fds251959}
}

@article{fds303796,
   Author = {Gianaros, PJ and Marsland, AL and Kuan, DC-H and Schirda, BL and Jennings, JR and Sheu, LK and Hariri, AR and Gross, JJ and Manuck,
             SB},
   Title = {An inflammatory pathway links atherosclerotic cardiovascular
             disease risk to neural activity evoked by the cognitive
             regulation of emotion.},
   Journal = {Biological Psychiatry},
   Volume = {75},
   Number = {9},
   Pages = {738-745},
   Year = {2014},
   Month = {May},
   ISSN = {0006-3223},
   url = {http://dx.doi.org/10.1016/j.biopsych.2013.10.012},
   Abstract = {Cognitive reappraisal is a form of emotion regulation that
             alters emotional responding by changing the meaning of
             emotional stimuli. Reappraisal engages regions of the
             prefrontal cortex that support multiple functions, including
             visceral control functions implicated in regulating the
             immune system. Immune activity plays a role in the
             preclinical pathophysiology of atherosclerotic
             cardiovascular disease (CVD), an inflammatory condition that
             is highly comorbid with affective disorders characterized by
             problems with emotion regulation. Here, we tested whether
             prefrontal engagement by reappraisal would be associated
             with atherosclerotic CVD risk and whether this association
             would be mediated by inflammatory activity.Community
             volunteers (n = 157; 30-54 years of age; 80 women) without
             DSM-IV Axis-1 psychiatric diagnoses or cardiovascular or
             immune disorders performed a functional neuroimaging task
             involving the reappraisal of negative emotional stimuli.
             Carotid artery intima-media thickness and inter-adventitial
             diameter were measured by ultrasonography and used as
             markers of preclinical atherosclerosis. Also measured were
             circulating levels of interleukin-6 (IL-6), an inflammatory
             cytokine linked to CVD risk and prefrontal neural
             activity.Greater reappraisal-related engagement of the
             dorsal anterior cingulate cortex was associated with greater
             preclinical atherosclerosis and IL-6. Moreover, IL-6
             mediated the association of dorsal anterior cingulate cortex
             engagement with preclinical atherosclerosis. These results
             were independent of age, sex, race, smoking status, and
             other known CVD risk factors.The cognitive regulation of
             emotion might relate to CVD risk through a pathway involving
             the functional interplay between the anterior cingulate
             region of the prefrontal cortex and inflammatory
             activity.},
   Doi = {10.1016/j.biopsych.2013.10.012},
   Key = {fds303796}
}

@article{fds251963,
   Author = {McCarty, CA and Huggins, W and Aiello, AE and Bilder, RM and Hariri, A and Jernigan, TL and Newman, E and Sanghera, DK and Strauman, TJ and Zeng,
             Y and Ramos, EM and Junkins, HA and PhenX RISING network},
   Title = {PhenX RISING: real world implementation and sharing of PhenX
             measures.},
   Journal = {BMC Medical Genomics},
   Volume = {7},
   Pages = {16},
   Year = {2014},
   Month = {March},
   url = {http://dx.doi.org/10.1186/1755-8794-7-16},
   Abstract = {The purpose of this manuscript is to describe the PhenX
             RISING network and the site experiences in the
             implementation of PhenX measures into ongoing
             population-based genomic studies.Eighty PhenX measures were
             implemented across the seven PhenX RISING groups,
             thirty-three of which were used at more than two sites,
             allowing for cross-site collaboration. Each site used
             between four and 37 individual measures and five of the
             sites are validating the PhenX measures through comparison
             with other study measures. Self-administered and
             computer-based administration modes are being evaluated at
             several sites which required changes to the original PhenX
             Toolkit protocols. A network-wide data use agreement was
             developed to facilitate data sharing and collaboration.PhenX
             Toolkit measures have been collected for more than 17,000
             participants across the PhenX RISING network. The process of
             implementation provided information that was used to improve
             the PhenX Toolkit. The Toolkit was revised to allow
             researchers to select self- or interviewer administration
             when creating the data collection worksheets and ranges of
             specimens necessary to run biological assays has been added
             to the Toolkit.The PhenX RISING network has demonstrated
             that the PhenX Toolkit measures can be implemented
             successfully in ongoing genomic studies. The next step will
             be to conduct gene/environment studies.},
   Doi = {10.1186/1755-8794-7-16},
   Key = {fds251963}
}

@article{fds251961,
   Author = {Hyde, LW and Byrd, AL and Votruba-Drzal, E and Hariri, AR and Manuck,
             SB},
   Title = {Amygdala reactivity and negative emotionality: divergent
             correlates of antisocial personality and psychopathy traits
             in a community sample.},
   Journal = {Journal of Abnormal Psychology},
   Volume = {123},
   Number = {1},
   Pages = {214-224},
   Year = {2014},
   Month = {February},
   ISSN = {0021-843X},
   url = {http://dx.doi.org/10.1037/a0035467},
   Abstract = {Previous studies have emphasized that antisocial personality
             disorder (APD) and psychopathy overlap highly but differ
             critically in several features, notably negative
             emotionality (NEM) and possibly amygdala reactivity to
             social signals of threat and distress. Here we examined
             whether dimensions of psychopathy and APD correlate
             differentially with NEM and amygdala reactivity to emotional
             faces. Testing these relationships among healthy
             individuals, dimensions of psychopathy and APD were
             generated by the profile matching technique of Lynam and
             Widiger (2001), using facet scales of the NEO Personality
             Inventory-Revised, and amygdala reactivity was measured
             using a well-established emotional faces task, in a
             community sample of 103 men and women. Higher psychopathy
             scores were associated with lower NEM and lower amygdala
             reactivity, whereas higher APD scores were related to
             greater NEM and greater amygdala reactivity, but only after
             overlapping variance in APD and psychopathy was adjusted for
             in the statistical model. Amygdala reactivity did not
             mediate the relationship of APD and psychopathy scores to
             NEM. Supplemental analyses also compared other measures of
             factors within psychopathy in predicting NEM and amygdala
             reactivity and found that Factor 2 psychopathy was
             positively related to NEM and amygdala reactivity across
             measures of psychopathy. The overall findings replicate
             seminal observations on NEM in psychopathy by Hicks and
             Patrick (2006) and extend this work to neuroimaging in a
             normative population. They also suggest that one critical
             way in which APD and psychopathy dimensions may differ in
             their etiology is through their opposing levels of NEM and
             amygdala reactivity to threat.},
   Doi = {10.1037/a0035467},
   Key = {fds251961}
}

@article{fds251965,
   Author = {Roses, AD and Saunders, AM and Lutz, MW and Zhang, N and Hariri, AR and Asin, KE and Crenshaw, DG and Budur, K and Burns, DK and Brannan,
             SK},
   Title = {New applications of disease genetics and pharmacogenetics to
             drug development.},
   Journal = {Current Opinion in Pharmacology},
   Volume = {14},
   Pages = {81-89},
   Year = {2014},
   Month = {February},
   ISSN = {1471-4892},
   url = {http://dx.doi.org/10.1016/j.coph.2013.12.002},
   Abstract = {TOMMORROW is a Phase III delay of onset clinical trial to
             determine whether low doses of pioglitazone, a molecule that
             induces mitochondrial doubling, delays the onset of MCI-AD
             in normal subjects treated with low dose compared to
             placebo. BOLD imaging studies in rodents and man were used
             to find the dose that increases oxygen consumption at
             central regions of the brain in higher proportion than
             activation of large corticol regions. The trial is made
             practical by the use of a pharmacogenetic algorithm based on
             TOMM40 and APOE genotypes and age to identify normal
             subjects at high risk of MCI-AD between the ages of 65-83
             years within a five year follow-up period.},
   Doi = {10.1016/j.coph.2013.12.002},
   Key = {fds251965}
}

@article{fds251967,
   Author = {Wellman, CL and Camp, M and Jones, VM and MacPherson, KP and Ihne, J and Fitzgerald, P and Maroun, M and Drabant, E and Bogdan, R and Hariri, AR and Holmes, A},
   Title = {Corrigendum to "Convergent effects of mouse Pet-1 deletion
             and human PET-1 variation on amygdala fear and threat
             processing" [Exp. Neurol. 250 (2013) 260-269]},
   Journal = {Experimental Neurology},
   Volume = {252},
   Pages = {104},
   Year = {2014},
   Month = {February},
   ISSN = {0014-4886},
   url = {http://dx.doi.org/10.1016/j.expneurol.2013.11.002},
   Doi = {10.1016/j.expneurol.2013.11.002},
   Key = {fds251967}
}

@article{fds251942,
   Author = {Gorka, AX and Hanson, JL and Radtke, SR and Hariri,
             AR},
   Title = {Reduced hippocampal and medial prefrontal gray matter
             mediate the association between reported childhood
             maltreatment and trait anxiety in adulthood and predict
             sensitivity to future life stress},
   Journal = {Biology of Mood and Anxiety Disorders},
   Volume = {4},
   Number = {1},
   Pages = {12-12},
   Year = {2014},
   ISSN = {2045-5380},
   url = {http://dx.doi.org/10.1186/2045-5380-4-12},
   Doi = {10.1186/2045-5380-4-12},
   Key = {fds251942}
}

@article{fds251968,
   Author = {Disner, SG and Beevers, CG and Lee, HJ and Ferrell, RE and Hariri, AR and Telch, MJ},
   Title = {War zone stress interacts with the 5-HTTLPR polymorphism to
             predict the development of sustained attention for negative
             emotion stimuli in soldiers returning from
             Iraq},
   Journal = {Clinical Psychological Science},
   Volume = {1},
   Number = {4},
   Pages = {413-425},
   Year = {2013},
   Month = {December},
   ISSN = {2167-7026},
   url = {http://dx.doi.org/10.1177/2167702613485564},
   Abstract = {Biased attention toward negative stimuli is a known
             vulnerability for affective psychopathology. However,
             factors that contribute to the development of this cognitive
             bias are largely unknown. Variation within t he serotonin
             transporter gene (i.e., 5-HTTLPR) is associated with
             increased susceptibility to environmental influence and
             biased processing of negative stimuli. Using a passive
             viewing eye-tracking paradigm, this study examined gaze
             fixation for emotion stimuli in 91 U.S. Army soldiers before
             and after deployment to Iraq. In addition, participants
             underwent genetic assay and provided in situ measures of war
             zone stress exposure. 5-HTTLPR short allele homozygotes were
             more likely than other genotype groups to develop a gaze
             bias toward negative stimuli as a function of increasing war
             zone stress, even when controlling for postdeployment
             posttraumatic stress disorder and depression severity. Short
             allele homozygotes appear especially sensitive to
             environmental influence, which likely contributes to the
             development of cognitive vulnerability to anxiety and mood
             disorders. © The Author(s) 2013.},
   Doi = {10.1177/2167702613485564},
   Key = {fds251968}
}

@article{Wellman2013,
   Author = {Wellman, CL and Camp, M and Jones, VM and MacPherson, KP and Ihne, J and Fitzgerald, P and Maroun, M and Drabant, E and Bogdan, R and Hariri, AR and Holmes, A},
   Title = {Convergent effects of mouse Pet-1 deletion and human PET-1
             variation on amygdala fear and threat processing},
   Journal = {Experimental Neurology},
   Volume = {250},
   Pages = {260-269},
   Address = {Department of Psychological and Brain Sciences, Center for
             the Integrative Study of Animal Behavior, Indiana
             University, Bloomington, IN, USA. Electronic address:
             wellmanc@indiana.edu.},
   Year = {2013},
   Month = {December},
   ISSN = {0014-4886},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/24100022},
   Abstract = {Serotonin is critical for shaping the development of neural
             circuits regulating emotion. Pet-1 (FEV-1) is an ETS-domain
             transcription factor essential for differentiation and
             forebrain targeting of serotonin neurons. Constitutive Pet-1
             knockout (KO) causes major loss of serotonin neurons and
             forebrain serotonin availability, and behavioral
             abnormalities. We phenotyped Pet-1 KO mice for fear
             conditioning and extinction, and on a battery of assays for
             anxiety- and depression-related behaviors. Morphology of
             Golgi-stained neurons in basolateral amygdala (BLA) and
             prelimbic cortex was examined. Using human imaging genetics,
             a common variant (rs860573) in the PET-1 (FEV) gene was
             tested for effects on threat-related amygdala reactivity and
             psychopathology in 88 Asian-ancestry subjects. Pet-1 KO mice
             exhibited increased acquisition and expression of fear, and
             elevated fear recovery following extinction, relative to
             wild-type (WT). BLA dendrites of Pet-1 KO mice were
             significantly longer than in WT. Human PET-1 variation
             associated with differences in amygdala threat processing
             and psychopathology. This novel evidence for the role of
             Pet-1 in fear processing and dendritic organization of
             amygdala neurons and in human amygdala threat processing
             extends a growing literature demonstrating the influence of
             genetic variation in the serotonin system on emotional
             regulation via effects on structure and function of
             underlying corticolimbic circuitry. © 2013 Elsevier
             Inc.},
   Language = {eng},
   Doi = {10.1016/j.expneurol.2013.09.025},
   Key = {Wellman2013}
}

@article{Davis2013,
   Author = {Davis, FC and Knodt, AR and Sporns, O and Lahey, BB and Zald, DH and Brigidi, BD and Hariri, AR},
   Title = {Impulsivity and the modular organization of resting-state
             neural networks.},
   Journal = {Cerebral Cortex},
   Volume = {23},
   Number = {6},
   Pages = {1444-1452},
   Address = {Laboratory of NeuroGenetics, Department of Psychology and
             Neuroscience, Duke University, Durham, NC 27708, USA.
             caroline.davis@duke.edu},
   Year = {2013},
   Month = {June},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/22645253},
   Keywords = {Adolescent • *Brain Mapping • Female • Head
             Movements • Humans • Image Processing,
             Computer-Assisted • Impulsive Behavior/classification/*pathology
             • Magnetic Resonance Imaging • Male • Models,
             Neurological • Neural Pathways/blood supply/*pathology
             • Oxygen • Rest/*physiology • Self Report
             • Young Adult},
   Abstract = {Impulsivity is a complex trait associated with a range of
             maladaptive behaviors, including many forms of
             psychopathology. Previous research has implicated multiple
             neural circuits and neurotransmitter systems in impulsive
             behavior, but the relationship between impulsivity and
             organization of whole-brain networks has not yet been
             explored. Using graph theory analyses, we characterized the
             relationship between impulsivity and the functional
             segregation ("modularity") of the whole-brain network
             architecture derived from resting-state functional magnetic
             resonance imaging (fMRI) data. These analyses revealed
             remarkable differences in network organization across the
             impulsivity spectrum. Specifically, in highly impulsive
             individuals, regulatory structures including medial and
             lateral regions of the prefrontal cortex were isolated from
             subcortical structures associated with appetitive drive,
             whereas these brain areas clustered together within the same
             module in less impulsive individuals. Further exploration of
             the modular organization of whole-brain networks revealed
             novel shifts in the functional connectivity between visual,
             sensorimotor, cortical, and subcortical structures across
             the impulsivity spectrum. The current findings highlight the
             utility of graph theory analyses of resting-state fMRI data
             in furthering our understanding of the neurobiological
             architecture of complex behaviors.},
   Language = {eng},
   Doi = {10.1093/cercor/bhs126},
   Key = {Davis2013}
}

@article{fds251962,
   Author = {Salazar, E and Bogdan, R and Gorka, A and Hariri, AR and Carin,
             L},
   Title = {Exploring the mind: Integrating questionnaires and
             fMRI},
   Journal = {30th International Conference on Machine Learning, ICML
             2013},
   Number = {PART 2},
   Pages = {921-929},
   Year = {2013},
   Month = {January},
   Abstract = {A new model is developed for joint analysis of ordered,
             categorical, real and count data. The ordered and
             categorical data are answers to questionnaires, the (word)
             count data correspond to the text questions from the
             questionnaires, and the real data correspond to fMRI
             responses for each subject. The Bayesian model employs the
             von Mises distribution in a novel manner to infer sparse
             graphical models jointly across people, questions, fMRI
             stimuli and brain region, with this integrated within a new
             matrix factorization based on latent binary features. The
             model is compared with simpler alternatives on two real
             datasets. We also demonstrate the ability to predict the
             response of the brain to visual stimuli (as measured by
             fMRI), based on knowledge of how the associated person
             answered classical questionnaires. Copyright 2013 by the
             author(s).},
   Key = {fds251962}
}

@article{Goetz2013,
   Author = {Goetz, E. L. and Hariri, A. R. and Pizzagalli, D. A. and Strauman, T. J.},
   Title = {Genetic moderation of the association between regulatory
             focus and reward responsiveness: a proof-of-concept
             study},
   Journal = {Biology of mood \& anxiety disorders},
   Volume = {3},
   Number = {1},
   Pages = {3},
   Address = {Department of Psychology \& Neuroscience, Duke University,
             Durham, NC, USA. elena.goetz@duke.edu.},
   Year = {2013},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/23369671},
   Abstract = {BACKGROUND: Recent studies implicate individual differences
             in regulatory focus as contributing to self-regulatory
             dysfunction, particularly not responding to positive
             outcomes. How such individual differences emerge, however,
             is unclear. We conducted a proof-of-concept study to examine
             the moderating effects of genetically driven variation in
             dopamine signaling, a key modulator of neural reward
             circuits, on the association between regulatory focus and
             reward cue responsiveness. METHOD: Healthy Caucasians (N=59)
             completed a measure of chronic regulatory focus and a
             probabilistic reward task. A common functional genetic
             polymorphism impacting prefrontal dopamine signaling (COMT
             rs4680) was evaluated. RESULTS: Response bias, the
             participants' propensity to modulate behavior as a function
             of reward, was predicted by an interaction of regulatory
             focus and COMT genotype. Specifically, self-perceived
             success at achieving promotion goals predicted total
             response bias, but only for individuals with the COMT
             genotype (Val/Val) associated with relatively increased
             phasic dopamine signaling and cognitive flexibility.
             CONCLUSIONS: The combination of success in promotion goal
             pursuit and Val/Val genotype appears to facilitate
             responding to reward opportunities in the environment. This
             study is among the first to integrate an assessment of
             self-regulatory style with an examination of genetic
             variability that underlies responsiveness to positive
             outcomes in goal pursuit.},
   Language = {eng},
   Doi = {10.1186/2045-5380-3-3},
   Key = {Goetz2013}
}

@article{Carre2013a,
   Author = {Carre, J. M. and Murphy, K. R. and Hariri, A.
             R.},
   Title = {What lies beneath the face of aggression?},
   Journal = {Social cognitive and affective neuroscience},
   Volume = {8},
   Number = {2},
   Pages = {224--9},
   Address = {Laboratory of NeuroGenetics, Department of Psychology and
             Neuroscience, Duke University, Durham, NC, USA.
             justin@carrelab.com},
   Year = {2013},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/22198969},
   Keywords = {Adult • Aggression/*physiology •
             Amygdala/*physiology • Anger/physiology •
             Anthropometry • *Face/anatomy \& histology/physiology
             • *Facial Expression • Fear/physiology •
             Female • Humans • Magnetic Resonance
             Imaging/instrumentation/*methods • Male •
             Neuroimaging/methods/psychology • Neuropsychological
             Tests • Sex Characteristics • Young
             Adult},
   Abstract = {Recent evidence indicates that a sexually dimorphic feature
             of humans, the facial width-to-height ratio (FWHR), is
             positively correlated with reactive aggression, particularly
             in men. Also, predictions about the aggressive tendencies of
             others faithfully map onto FWHR in the absence of explicit
             awareness of this metric. Here, we provide the first
             evidence that amygdala reactivity to social signals of
             interpersonal challenge may underlie the link between
             aggression and the FWHR. Specifically, amygdala reactivity
             to angry faces was positively correlated with aggression,
             but only among men with relatively large FWHRs. The patterns
             of association were specific to angry facial expressions and
             unique to men. These links may reflect the common influence
             of pubertal testosterone on craniofacial growth and
             development of neural circuitry underlying aggression.
             Amygdala reactivity may also represent a plausible pathway
             through which FWHR may have evolved to represent an honest
             indicator of conspecific threat, namely by reflecting the
             responsiveness of neural circuitry mediating aggressive
             behavior.},
   Language = {eng},
   Doi = {10.1093/scan/nsr096},
   Key = {Carre2013a}
}

@article{Gianaros2013,
   Author = {Gianaros, PJ and Marsland, AL and Kuan, DC-H and Schirda, BL and Jennings, JR and Sheu, LK and Hariri, AR and Gross, JJ and Manuck,
             SB},
   Title = {An Inflammatory Pathway Links Atherosclerotic Cardiovascular
             Disease Risk to Neural Activity Evoked by the Cognitive
             Regulation of Emotion},
   Journal = {Biological Psychiatry},
   Volume = {75},
   Number = {9},
   Pages = {738-745},
   Address = {Department of Psychology (PJG, ALM, DC-HK, LKS, SBM).
             Electronic address: gianaros@pitt.edu.},
   Year = {2013},
   ISSN = {0006-3223},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/24267410},
   Abstract = {BACKGROUND: Cognitive reappraisal is a form of emotion
             regulation that alters emotional responding by changing the
             meaning of emotional stimuli. Reappraisal engages regions of
             the prefrontal cortex that support multiple functions,
             including visceral control functions implicated in
             regulating the immune system. Immune activity plays a role
             in the preclinical pathophysiology of atherosclerotic
             cardiovascular disease (CVD), an inflammatory condition that
             is highly comorbid with affective disorders characterized by
             problems with emotion regulation. Here, we tested whether
             prefrontal engagement by reappraisal would be associated
             with atherosclerotic CVD risk and whether this association
             would be mediated by inflammatory activity. METHODS:
             Community volunteers (n = 157; 30-54 years of age; 80 women)
             without DSM-IV Axis-1 psychiatric diagnoses or
             cardiovascular or immune disorders performed a functional
             neuroimaging task involving the reappraisal of negative
             emotional stimuli. Carotid artery intima-media thickness and
             inter-adventitial diameter were measured by ultrasonography
             and used as markers of preclinical atherosclerosis. Also
             measured were circulating levels of interleukin-6 (IL-6), an
             inflammatory cytokine linked to CVD risk and prefrontal
             neural activity. RESULTS: Greater reappraisal-related
             engagement of the dorsal anterior cingulate cortex was
             associated with greater preclinical atherosclerosis and
             IL-6. Moreover, IL-6 mediated the association of dorsal
             anterior cingulate cortex engagement with preclinical
             atherosclerosis. These results were independent of age, sex,
             race, smoking status, and other known CVD risk factors.
             CONCLUSIONS: The cognitive regulation of emotion might
             relate to CVD risk through a pathway involving the
             functional interplay between the anterior cingulate region
             of the prefrontal cortex and inflammatory
             activity.},
   Language = {Eng},
   Doi = {10.1016/j.biopsych.2013.10.012},
   Key = {Gianaros2013}
}

@article{Hyde2013,
   Author = {Hyde, LW and Shaw, DS and Hariri, AR},
   Title = {Understanding youth antisocial behavior using neuroscience
             through a developmental psychopathology lens: Review,
             integration, and directions for research},
   Journal = {Developmental Review},
   Volume = {33},
   Number = {3},
   Pages = {168-223},
   Address = {University of Michigan.},
   Year = {2013},
   ISSN = {0273-2297},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/24273368},
   Abstract = {Youth antisocial behavior (AB) is an important public health
             concern impacting perpetrators, victims, and society.
             Functional neuroimaging is becoming a more common and useful
             modality for understanding neural correlates of youth AB.
             Although there has been a recent increase in neuroimaging
             studies of youth AB and corresponding theoretical articles
             on the neurobiology of AB, there has been little work
             critically examining the strengths and weaknesses of
             individual studies and using this knowledge to inform the
             design of future studies. Additionally, research on
             neuroimaging and youth AB has not been integrated within the
             broader framework of developmental psychopathology. Thus,
             this paper provides an in-depth review of the youth AB
             functional neuroimaging literature with the following goals:
             (1) to evaluate how this literature has informed our
             understanding of youth AB, (2) to evaluate current
             neuroimaging studies of youth AB from a developmental
             psychopathology perspective with a focus on integrating
             research from neuroscience and developmental
             psychopathology, as well as placing this research in the
             context of other related areas (e.g., psychopathy, molecular
             genetics), and (3) to examine strengths and weaknesses of
             neuroimaging and behavioral studies of youth AB to suggest
             how future studies can develop a more informed and
             integrated understanding of youth AB. © 2013 Elsevier
             Inc.},
   Language = {Eng},
   Doi = {10.1016/j.dr.2013.06.001},
   Key = {Hyde2013}
}

@article{Zuurbier2013,
   Author = {Zuurbier, LA and Nikolova, YS and Ahs, F and Hariri,
             AR},
   Title = {Uncinate fasciculus fractional anisotropy correlates with
             typical use of reappraisal in women but not
             men},
   Journal = {Emotion},
   Volume = {13},
   Number = {3},
   Pages = {385-390},
   Address = {Laboratory of NeuroGenetics, Department of Psychology \&
             Neuroscience, Institute for Genome Sciences \& Policy, Duke
             University, Durham, NC, USA.},
   Year = {2013},
   ISSN = {1528-3542},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/23398586},
   Abstract = {Emotion regulation refers to strategies through which
             individuals influence their experience and expression of
             emotions. Two typical strategies are reappraisal, a
             cognitive strategy for reframing the context of an emotional
             experience, and suppression, a behavioral strategy for
             inhibiting emotional responses. Functional neuroimaging
             studies have revealed that regions of the prefrontal cortex
             modulate amygdala reactivity during both strategies, but
             relatively greater downregulation of the amygdala occurs
             during reappraisal. Moreover, these studies demonstrated
             that engagement of this modulatory circuitry varies as a
             function of gender. The uncinate fasciculus is a major
             structural pathway connecting regions of the anterior
             temporal lobe, including the amygdala to inferior frontal
             regions, especially the orbitofrontal cortex. The objective
             of the current study was to map variability in the
             structural integrity of the uncinate fasciculus onto
             individual differences in self-reported typical use of
             reappraisal and suppression. Diffusion tensor imaging was
             used in 194 young adults to derive regional fractional
             anisotropy values for the right and left uncinate
             fasciculus. All participants also completed the Emotion
             Regulation Questionnaire. In women but not men,
             self-reported typical reappraisal use was positively
             correlated with fractional anisotropy values in a region of
             the left uncinate fasciculus within the orbitofrontal
             cortex. In contrast, typical use of suppression was not
             significantly correlated with fractional anisotropy in any
             region of the uncinate fasciculus in either men or women.
             Our data suggest that in women typical reappraisal use is
             specifically related to the integrity of white matter
             pathways linking the amygdala and prefrontal cortex. © 2013
             American Psychological Association.},
   Language = {eng},
   Doi = {10.1037/a0031163},
   Key = {Zuurbier2013}
}

@article{Nikolova2013,
   Author = {Nikolova, YS and Singhi, EK and Drabant, EM and Hariri,
             AR},
   Title = {Reward-related ventral striatum reactivity mediates
             gender-specific effects of a galanin remote enhancer
             haplotype on problem drinking},
   Journal = {Genes, Brain and Behavior},
   Volume = {12},
   Number = {5},
   Pages = {516-524},
   Address = {Laboratory of NeuroGenetics, Department of Psychology and
             Neuroscience; Institute for Genome Sciences \& Policy, Duke
             University, Durham, NC 27705, USA. yuliya.nikolova@duke.edu},
   Year = {2013},
   ISSN = {1601-1848},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/23489876},
   Abstract = {The neuropeptide galanin has been implicated in the
             regulation of appetitive and consummatory behaviors. Prior
             studies have shown that direct injection of galanin into the
             hypothalamus results in increased release of dopamine (DA)
             in the nucleus accumbens (NAcc), and parallel increases in
             food and alcohol consumption. These studies are consistent
             with a role of hypothalamic galanin in regulating reward
             system reactivity. In humans, a common functional haplotype
             (GAL5.1) within a remote enhancer region upstream of the
             galanin gene (GAL) affects promoter activity and galanin
             expression in hypothalamic neurons in vitro. Given the
             effects of hypothalamic galanin on NAcc DA release and the
             effects of the GAL5.1 haplotype on GAL expression, we
             examined the impact of this functional genetic variation on
             human reward-related ventral striatum (VS) reactivity. Using
             an imaging genetics strategy in Caucasian individuals
             (N=138, 72 women) participating in the ongoing Duke
             Neurogenetics Study, we report a significant
             gender-by-genotype interaction (right hemisphere:
             F1,134=8.08, P=0.005; left hemisphere: F1,134=5.39,
             P=0.022), such that homozygosity for the GG haplotype, which
             predicts greater GAL expression, is associated with
             relatively increased VS reactivity in women (n=50, right
             hemisphere: P=0.015; left hemisphere: P=0.060), but not in
             men (N=49, P-values&gt;0.10). Furthermore, these differences
             in VS reactivity correlated positively with differences in
             alcohol use, such that VS reactivity mediated a
             gender-specific association between GAL5.1 haplotype and
             problem drinking. Our current results support those in
             animal models implicating galanin signaling in neural
             pathways associated with appetitive and consummatory
             behaviors of relevance for understanding risk for substance
             use and abuse. © 2013 John Wiley &amp; Sons Ltd and
             International Behavioural and Neural Genetics
             Society.},
   Language = {eng},
   Doi = {10.1111/gbb.12035},
   Key = {Nikolova2013}
}

@article{Prather2013,
   Author = {Prather, AA and Bogdan, R and Hariri, AR},
   Title = {Impact of sleep quality on amygdala reactivity, negative
             affect, and perceived stress},
   Journal = {Psychosomatic Medicine},
   Volume = {75},
   Number = {4},
   Pages = {350-358},
   Address = {Department of Psychiatry, University of California, San
             Francisco, CA, USA. prathera@chc.ucsf.edu},
   Year = {2013},
   ISSN = {0033-3174},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/23592753},
   Keywords = {Adolescent • Adult • Affect/*physiology •
             Amygdala/*physiopathology • Anger •
             Anxiety/physiopathology/psychology •
             Depression/physiopathology/psychology • Facial
             Expression • Fear • Female • Humans •
             *Magnetic Resonance Imaging • Male • Self Report
             • Severity of Illness Index • Sex Factors •
             Sleep/*physiology • Sleep Disorders/*physiopathology/psychology
             • Stress, Psychological/etiology/*physiopathology
             • Visual Cortex/physiopathology • Young
             Adult},
   Abstract = {OBJECTIVE: Research demonstrates a negative impact of sleep
             disturbance on mood and affect; however, the biological
             mechanisms mediating these links are poorly understood.
             Amygdala reactivity to negative stimuli has emerged as one
             potential pathway. Here, we investigate the influence of
             self-reported sleep quality on associations between
             threat-related amygdala reactivity and measures of negative
             affect and perceived stress. METHODS: Analyses on data from
             299 participants (125 men, 50.5% white, mean [standard
             deviation] age = 19.6 [1.3] years) who completed the Duke
             Neurogenetics Study were conducted. Participants completed
             several self-report measures of negative affect and
             perceived stress. Threat-related (i.e., angry and fearful
             facial expressions) amygdala reactivity was assayed using
             blood oxygen level-dependent functional magnetic resonance
             imaging. Global sleep quality was assessed using the
             Pittsburgh Sleep Quality Index. RESULTS: Amygdala reactivity
             to fearful facial expressions predicted greater depressive
             symptoms and higher perceived stress in poor (β values =
             0.18-1.86, p values &lt; .05) but not good sleepers (β
             values = -0.13 to -0.01, p values &gt; .05). In sex-specific
             analyses, men reporting poorer global sleep quality showed a
             significant association between amygdala reactivity and
             levels of depression and perceived stress (β values =
             0.29-0.44, p values &lt; .05). In contrast, no significant
             associations were observed in men reporting good global
             sleep quality or in women, irrespective of sleep quality.
             CONCLUSIONS: This study provides novel evidence that
             self-reported sleep quality moderates the relationships
             between amygdala reactivity, negative affect, and perceived
             stress, particularly among men. Copyright © 2013 by the
             American Psychosomatic Society.},
   Language = {eng},
   Doi = {10.1097/PSY.0b013e31828ef15b},
   Key = {Prather2013}
}

@article{Kienast2013,
   Author = {Kienast, T and Schlagenhauf, F and Rapp, MA and Wrase, J and Daig, I and Buchholz, H-G and Smolka, MN and Gründer, G and Kumakura, Y and Cumming, P and Charlet, K and Bartenstein, P and Hariri, AR and Heinz,
             A},
   Title = {Dopamine-modulated aversive emotion processing fails in
             alcohol-dependent patients},
   Journal = {Pharmacopsychiatry},
   Volume = {46},
   Number = {4},
   Pages = {130-136},
   Address = {Department of Psychiatry and Psychotherapy, Campus Charite
             Mitte, -Charite - Universitatsmedizin Berlin, Berlin,
             Germany.},
   Year = {2013},
   ISSN = {0176-3679},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/23364872},
   Abstract = {Introduction: Negative mood states after alcohol
             detoxification may enhance the relapse risk. As recently
             shown in healthy volunteers, dopamine storage capacity (V d)
             in the left amygdala was positively correlated with
             functional activation in the left amygdala and anterior
             cingulate cortex (ACC) during an emotional task; high
             functional connectivity between the amygdala and the ACC, a
             region important for emotion regulation, was associated with
             low trait anxiety. Based on these findings, we now tested
             whether detoxified alcohol-dependent patients have a
             disrupted modulation of the anterior cingulate cortex
             activation in response to aversive stimuli by amygdala
             dopamine. Furthermore, we asked whether disrupted functional
             coupling between amygdala and ACC during aversive processing
             is related to trait anxiety. Methods: We used combined
             6-[18F]-fluoro-l-DOPA positron emission tomography (PET),
             functional magnetic resonance imaging (fMRI) and
             Spielberger's state-trait anxiety questionnaire (STAI) in 11
             male detoxified alcohol-dependent patients compared to 13
             matched healthy controls. Results: Unlike healthy controls,
             patients showed no significant correlation between our PET
             metric for dopamine storage capacity (FDOPA V d), in left
             amygdala and activation in left ACC. Moreover, the
             functional connectivity between amygdala and ACC during
             processing of aversive emotional stimuli was reduced in
             patients. Voxel-based morphometry did not reveal any
             discernible group differences in amygdala volume.
             Discussion: These results suggest that dopamine-modulated
             corticolimbic circuit function is important for responding
             to emotional information such that apparent functional
             deficits in this neuromodulatory circuitry may contribute to
             trait anxiety in alcohol-dependent patients. © Georg Thieme
             Verlag KG Stuttgart New York.},
   Language = {eng},
   Doi = {10.1055/s-0032-1331747},
   Key = {Kienast2013}
}

@article{Fisher2013,
   Author = {Fisher, PM and Hariri, AR},
   Title = {Identifying serotonergic mechanisms underlying the
             corticolimbic response to threat in humans},
   Journal = {Philosophical Transactions B},
   Volume = {368},
   Number = {1615},
   Pages = {20120192-},
   Address = {Center for Integrated Molecular Brain Imaging, University of
             Copenhagen, Copenhagen 2100, Denmark. patrick.fisher@nru.dk},
   Year = {2013},
   ISSN = {0962-8436},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/23440464},
   Keywords = {Amygdala/drug effects/*metabolism/physiology •
             Antidepressive Agents/pharmacology • Depression/drug
             therapy/physiopathology • Fear/*physiology •
             Humans • Neural Pathways/metabolism/physiology •
             Neuroimaging • Personality/physiology • Prefrontal
             Cortex/*metabolism/physiology • Protein Binding •
             Receptor, Serotonin, 5-HT1A/metabolism •
             Serotonin/*metabolism • Serotonin Uptake
             Inhibitors/pharmacology},
   Abstract = {A corticolimbic circuit including the amygdala and medial
             prefrontal cortex (mPFC) plays an important role in
             regulating sensitivity to threat, which is heightened in
             mood and anxiety disorders. Serotonin is a potent
             neuromodulator of this circuit; however, specific
             serotonergic mechanisms mediating these effects are not
             fully understood. Recent studies have evaluated molecular
             mechanisms mediating the effects of serotonin signalling on
             corticolimbic circuit function using a multi-modal
             neuroimaging strategy incorporating positron emission
             tomography and blood oxygen level-dependent functional
             magnetic resonance imaging. This multi-modal neuroimaging
             strategy can be integrated with additional techniques
             including imaging genetics and pharmacological challenge
             paradigms to more clearly understand how serotonin
             signalling modulates neural pathways underlying sensitivity
             to threat. Integrating these methodological approaches
             offers novel opportunities to identify mechanisms through
             which serotonin signalling contributes to differences in
             brain function and behaviour, which in turn can illuminate
             factors that confer risk for illness and inform the
             development of more effective treatment strategies. © 2013
             The Author(s) Published by the Royal Society. All rights
             reserved.},
   Language = {eng},
   Doi = {10.1098/rstb.2012.0192},
   Key = {Fisher2013}
}

@article{Lohoff2013,
   Author = {Lohoff, FW and Hodge, R and Narasimhan, S and Nall, A and Ferraro, TN and Mickey, BJ and Heitzeg, MM and Langenecker, SA and Zubieta, J-K and Bogdan, R and al, E},
   Title = {Functional genetic variants in the vesicular monoamine
             transporter 1 modulate emotion processing},
   Journal = {Molecular Psychiatry},
   Volume = {19},
   Number = {1},
   Pages = {129-139},
   Address = {Translational Research Laboratories, Department of
             Psychiatry, Center for Neurobiology and Behavior, University
             of Pennsylvania School of Medicine, Philadelphia, PA,
             USA.},
   Year = {2013},
   ISSN = {1359-4184},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/23337945},
   Abstract = {Emotional behavior is in part heritable and often disrupted
             in psychopathology. Identification of specific genetic
             variants that drive this heritability may provide important
             new insight into molecular and neurobiological mechanisms
             involved in emotionality. Our results demonstrate that the
             presynaptic vesicular monoamine transporter 1 (VMAT1)
             Thr136Ile (rs1390938) polymorphism is functional in vitro,
             with the Ile allele leading to increased monoamine transport
             into presynaptic vesicles. Moreover, we show that the
             Thr136Ile variant predicts differential responses in
             emotional brain circuits consistent with its effects in
             vitro. Lastly, deep sequencing of bipolar disorder (BPD)
             patients and controls identified several rare novel VMAT1
             variants. The variant Phe84Ser was only present in
             individuals with BPD and leads to marked increase monoamine
             transport in vitro. Taken together, our data show that VMAT1
             polymorphisms influence monoamine signaling, the functional
             response of emotional brain circuits and risk for
             psychopathology.Molecular Psychiatry advance online
             publication, 22 January 2013; doi:10.1038/mp.2012.193.},
   Language = {Eng},
   Doi = {10.1038/mp.2012.193},
   Key = {Lohoff2013}
}

@article{Gunduz-Cinar2013,
   Author = {Gunduz-Cinar, O and MacPherson, KP and Cinar, R and Gamble-George, J and Sugden, K and Williams, B and Godlewski, G and Ramikie, TS and Gorka,
             AX and Alapafuja, SO and Nikas, SP and Makriyannis, A and Poulton, R and Patel, S and Hariri, AR and Caspi, A and Moffitt, TE and Kunos, G and Holmes, A},
   Title = {Convergent translational evidence of a role for anandamide
             in amygdala-mediated fear extinction, threat processing and
             stress-reactivity},
   Journal = {Molecular Psychiatry},
   Volume = {18},
   Number = {7},
   Pages = {813-823},
   Address = {Laboratory of Behavioral and Genomic Neuroscience, Section
             on Behavioral and Genomic Neuroscience, National Institute
             on Alcoholism and Alcohol Abuse, NIH, Bethesda, MD,
             USA.},
   Year = {2013},
   ISSN = {1359-4184},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/22688188},
   Abstract = {Endocannabinoids are released 'on-demand' on the basis of
             physiological need, and can be pharmacologically augmented
             by inhibiting their catabolic degradation. The
             endocannabinoid anandamide is degraded by the catabolic
             enzyme fatty acid amide hydrolase (FAAH). Anandamide is
             implicated in the mediation of fear behaviors, including
             fear extinction, suggesting that selectively elevating brain
             anandamide could modulate plastic changes in fear. Here we
             first tested this hypothesis with preclinical experiments
             employing a novel, potent and selective FAAH inhibitor,
             AM3506 (5-(4-hydroxyphenyl)pentanesulfonyl fluoride).
             Systemic AM3506 administration before extinction decreased
             fear during a retrieval test in a mouse model of impaired
             extinction. AM3506 had no effects on fear in the absence of
             extinction training, or on various non-fear-related
             measures. Anandamide levels in the basolateral amygdala were
             increased by extinction training and augmented by systemic
             AM3506, whereas application of AM3506 to amygdala slices
             promoted long-term depression of inhibitory transmission, a
             form of synaptic plasticity linked to extinction. Further
             supporting the amygdala as effect-locus, the fear-reducing
             effects of systemic AM3506 were blocked by intra-amygdala
             infusion of a CB1 receptor antagonist and were fully
             recapitulated by intra-amygdala infusion of AM3506. On the
             basis of these preclinical findings, we hypothesized that
             variation in the human FAAH gene would predict individual
             differences in amygdala threat-processing and stress-coping
             traits. Consistent with this, carriers of a low-expressing
             FAAH variant (385A allele; rs324420) exhibited quicker
             habituation of amygdala reactivity to threat, and had lower
             scores on the personality trait of stress-reactivity. Our
             findings show that augmenting amygdala anandamide enables
             extinction-driven reductions in fear in mouse and may
             promote stress-coping in humans. © 2013 Macmillan
             Publishers Limited. All rights reserved.},
   Language = {eng},
   Doi = {10.1038/mp.2012.72},
   Key = {Gunduz-Cinar2013}
}

@article{fds311287,
   Author = {Bogdan, R and Hyde, LW and Hariri, AR},
   Title = {A neurogenetics approach to understanding individual
             differences in brain, behavior, and risk for
             psychopathology},
   Journal = {Molecular Psychiatry},
   Volume = {18},
   Number = {3},
   Pages = {288-299},
   Year = {2013},
   ISSN = {1359-4184},
   url = {http://dx.doi.org/10.1038/mp.2012.35},
   Abstract = {Neurogenetics research has begun to advance our
             understanding of how genetic variation gives rise to
             individual differences in brain function, which, in turn,
             shapes behavior and risk for psychopathology. Despite these
             advancements, neurogenetics research is currently confronted
             by three major challenges: (1) conducting research on
             individual variables with small effects, (2) absence of
             detailed mechanisms, and (3) a need to translate findings
             toward greater clinical relevance. In this review, we
             showcase techniques and developments that address these
             challenges and highlight the benefits of a neurogenetics
             approach to understanding brain, behavior and
             psychopathology. To address the challenge of small effects,
             we explore approaches including incorporating the
             environment, modeling epistatic relationships and using
             multilocus profiles. To address the challenge of mechanism,
             we explore how non-human animal research, epigenetics
             research and genome-wide association studies can inform our
             mechanistic understanding of behaviorally relevant brain
             function. Finally, to address the challenge of clinical
             relevance, we examine how neurogenetics research can
             identify novel therapeutic targets and for whom treatments
             work best. By addressing these challenges, neurogenetics
             research is poised to exponentially increase our
             understanding of how genetic variation interacts with the
             environment to shape the brain, behavior and risk for
             psychopathology. © 2013 Macmillan Publishers
             Limited.},
   Doi = {10.1038/mp.2012.35},
   Key = {fds311287}
}

@article{fds324857,
   Author = {Bogdan, R and Hyde, LW and Hariri, AR},
   Title = {A neurogenetics approach to understanding individual
             differences in brain, behavior, and risk for
             psychopathology},
   Journal = {Molecular Psychiatry},
   Volume = {18},
   Number = {3},
   Pages = {288-299},
   Year = {2013},
   url = {http://dx.doi.org/10.1038/mp.2012.35},
   Abstract = {Neurogenetics research has begun to advance our
             understanding of how genetic variation gives rise to
             individual differences in brain function, which, in turn,
             shapes behavior and risk for psychopathology. Despite these
             advancements, neurogenetics research is currently confronted
             by three major challenges: (1) conducting research on
             individual variables with small effects, (2) absence of
             detailed mechanisms, and (3) a need to translate findings
             toward greater clinical relevance. In this review, we
             showcase techniques and developments that address these
             challenges and highlight the benefits of a neurogenetics
             approach to understanding brain, behavior and
             psychopathology. To address the challenge of small effects,
             we explore approaches including incorporating the
             environment, modeling epistatic relationships and using
             multilocus profiles. To address the challenge of mechanism,
             we explore how non-human animal research, epigenetics
             research and genome-wide association studies can inform our
             mechanistic understanding of behaviorally relevant brain
             function. Finally, to address the challenge of clinical
             relevance, we examine how neurogenetics research can
             identify novel therapeutic targets and for whom treatments
             work best. By addressing these challenges, neurogenetics
             research is poised to exponentially increase our
             understanding of how genetic variation interacts with the
             environment to shape the brain, behavior and risk for
             psychopathology. © 2013 Macmillan Publishers
             Limited.},
   Doi = {10.1038/mp.2012.35},
   Key = {fds324857}
}

@article{fds318718,
   Author = {Fisher, PM and Hariri, AR},
   Title = {Identifying serotonergic mechanisms underlying the
             corticolimbic response to threat in humans.},
   Journal = {Philosophical Transactions B},
   Volume = {368},
   Number = {1615},
   Pages = {20120192-},
   Year = {2013},
   url = {http://dx.doi.org/10.1098/rstb.2012.0192},
   Abstract = {A corticolimbic circuit including the amygdala and medial
             prefrontal cortex (mPFC) plays an important role in
             regulating sensitivity to threat, which is heightened in
             mood and anxiety disorders. Serotonin is a potent
             neuromodulator of this circuit; however, specific
             serotonergic mechanisms mediating these effects are not
             fully understood. Recent studies have evaluated molecular
             mechanisms mediating the effects of serotonin signalling on
             corticolimbic circuit function using a multi-modal
             neuroimaging strategy incorporating positron emission
             tomography and blood oxygen level-dependent functional
             magnetic resonance imaging. This multi-modal neuroimaging
             strategy can be integrated with additional techniques
             including imaging genetics and pharmacological challenge
             paradigms to more clearly understand how serotonin
             signalling modulates neural pathways underlying sensitivity
             to threat. Integrating these methodological approaches
             offers novel opportunities to identify mechanisms through
             which serotonin signalling contributes to differences in
             brain function and behaviour, which in turn can illuminate
             factors that confer risk for illness and inform the
             development of more effective treatment strategies.},
   Doi = {10.1098/rstb.2012.0192},
   Key = {fds318718}
}

@article{Nikolova2012b,
   Author = {Nikolova, YS and Bogdan, R and Brigidi, BD and Hariri,
             AR},
   Title = {Ventral striatum reactivity to reward and recent life stress
             interact to predict positive affect.},
   Journal = {Biological Psychiatry},
   Volume = {72},
   Number = {2},
   Pages = {157-163},
   Address = {Department of Psychology and Neuroscience and Institute for
             Genome Sciences and Policy, Duke University, Durham, NC
             27705, USA. yuliya.nikolova@duke.edu},
   Year = {2012},
   Month = {July},
   ISSN = {0006-3223},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/22534456},
   Keywords = {Adult • Affect/*physiology • Brain
             Mapping/methods/*psychology • Corpus Striatum/blood
             supply/*physiology • Depressive Disorder,
             Major/*physiopathology • Ethnic Groups/psychology
             • Female • Humans • Life Change Events •
             Magnetic Resonance Imaging/methods/psychology • Male
             • *Reward • Self Report • Stress,
             Psychological/*physiopathology},
   Abstract = {BACKGROUND: Stressful life events are among the most
             reliable precipitants of major depressive disorder; yet, not
             everyone exposed to stress develops depression. It has been
             hypothesized that robust neural reactivity to reward and
             associated stable levels of positive affect (PA) may protect
             against major depressive disorder in the context of
             environmental adversity. However, little empirical data
             exist to confirm this postulation. Here, we test the
             hypothesis that individuals with relatively low ventral
             striatum (VS) reactivity to reward will show low PA levels
             in the context of recent life stress, while those with
             relatively high VS reactivity will be protected against
             these potentially depressogenic effects. METHODS:
             Differential VS reactivity to positive feedback was assessed
             using blood oxygen level-dependent functional magnetic
             resonance imaging in a sample of 200 nonpatient young
             adults. Recent life stress, current depressive symptoms, and
             PA were assessed via self-report. Linear regression models
             were used to investigate the moderating effects of VS
             reactivity on the relationship between recent stress and
             state PA across participants. RESULTS: Recent life stress
             interacted with VS reactivity to predict self-reported state
             PA, such that higher levels of life stress were associated
             with lower PA for participants with relatively low, but not
             for those with high, VS reactivity. These effects were
             independent of age, gender, race/ethnicity, trait PA, and
             early childhood trauma. CONCLUSIONS: The current results
             provide empirical evidence for the potentially protective
             role of robust reward-related neural responsiveness against
             reductions in PA that may occur in the wake of life stress
             and possibly vulnerability to depression precipitated by
             stressful life events.},
   Language = {eng},
   Doi = {10.1016/j.biopsych.2012.03.014},
   Key = {Nikolova2012b}
}

@article{Sweitzer2012,
   Author = {Sweitzer, MM and Donny, EC and Hariri, AR},
   Title = {Imaging genetics and the neurobiological basis of individual
             differences in vulnerability to addiction.},
   Journal = {Drug and Alcohol Dependence},
   Volume = {123 Suppl 1},
   Number = {SUPPL.1},
   Pages = {S59-S71},
   Address = {Department of Psychology, University of Pittsburgh,
             Pittsburgh, PA 15260, USA. mms74@pitt.edu},
   Year = {2012},
   Month = {June},
   ISSN = {0376-8716},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/22342427},
   Keywords = {Adult • Basal Ganglia/drug effects • Behavior,
             Addictive/*genetics/physiopathology • Genetic
             Variation/*physiology • Humans • Impulsive
             Behavior/*genetics/psychology • Individuality •
             Male • Neural Pathways/*physiopathology •
             *Neuroimaging • Phenotype • Polymorphism,
             Genetic/physiology • Receptors, Dopamine
             D2/*genetics/physiology • Tobacco Use
             Disorder/*genetics/physiopathology},
   Abstract = {Addictive disorders are heritable, but the search for
             candidate functional polymorphisms playing an etiological
             role in addiction is hindered by complexity of the phenotype
             and the variety of factors interacting to impact behavior.
             Advances in human genome sequencing and neuroimaging
             technology provide an unprecedented opportunity to explore
             the impact of functional genetic variants on variability in
             behaviorally relevant neural circuitry. Here, we present a
             model for merging these technologies to trace the links
             between genes, brain, and addictive behavior.We describe
             imaging genetics and discuss the utility of its application
             to addiction. We then review data pertaining to impulsivity
             and reward circuitry as an example of how genetic variation
             may lead to variation in behavioral phenotype. Finally, we
             present preliminary data relating the neural basis of reward
             processing to individual differences in nicotine
             dependence.Complex human behaviors such as addiction can be
             traced to their basic genetic building blocks by identifying
             intermediate behavioral phenotypes, associated neural
             circuitry, and underlying molecular signaling pathways.
             Impulsivity has been linked with variation in reward-related
             activation in the ventral striatum (VS), altered dopamine
             signaling, and functional polymorphisms of DRD2 and DAT1
             genes. In smokers, changes in reward-related VS activation
             induced by smoking abstinence may be associated with
             severity of nicotine dependence.Variation in genes related
             to dopamine signaling may contribute to heterogeneity in VS
             sensitivity to reward and, ultimately, to addiction. These
             findings illustrate the utility of the imaging genetics
             approach for investigating the neurobiological basis for
             vulnerability to addiction.},
   Language = {eng},
   Doi = {10.1016/j.drugalcdep.2012.01.017},
   Key = {Sweitzer2012}
}

@article{Fisher2012,
   Author = {Fisher, PM and Hariri, AR},
   Title = {Linking variability in brain chemistry and circuit function
             through multimodal human neuroimaging},
   Journal = {Genes, Brain and Behavior},
   Volume = {11},
   Number = {6},
   Pages = {633-642},
   Address = {Center for Integrated Molecular Brain Imaging, Copenhagen
             University Hospital Rigshospitalet, Copenhagen, Denmark.
             patrick.fisher@gmail.com},
   Year = {2012},
   ISSN = {1601-1848},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/22443230},
   Keywords = {Brain/physiology/radionuclide imaging • Brain
             Chemistry/genetics/*physiology • Brain
             Diseases/genetics/*physiopathology/*radionuclide imaging
             • Humans • Magnetic Resonance Imaging/methods
             • Neuroimaging/*methods • Positron-Emission
             Tomography/*methods},
   Abstract = {Identifying neurobiological mechanisms mediating the
             emergence of individual differences in behavior is critical
             for advancing our understanding of relative risk for
             psychopathology. Neuroreceptor positron emission tomography
             (PET) and functional magnetic resonance imaging (fMRI) can
             be used to assay in vivo regional brain chemistry and
             function, respectively. Typically, these neuroimaging
             modalities are implemented independently despite the
             capacity for integrated data sets to offer unique insight
             into molecular mechanisms associated with brain function.
             Through examples from the serotonin and dopamine system and
             its effects on threat- and reward-related brain function, we
             review evidence for how such a multimodal neuroimaging
             strategy can be successfully implemented. Furthermore, we
             discuss how multimodal PET-fMRI can be integrated with
             techniques such as imaging genetics, pharmacological
             challenge paradigms and gene-environment interaction models
             to more completely map biological pathways mediating
             individual differences in behavior and related risk for
             psychopathology and inform the development of novel
             therapeutic targets. © 2012 Blackwell Publishing Ltd and
             International Behavioural and Neural Genetics
             Society.},
   Language = {eng},
   Doi = {10.1111/j.1601-183X.2012.00786.x},
   Key = {Fisher2012}
}

@article{Bogdan2013,
   Author = {Bogdan, R and Hyde, LW and Hariri, AR},
   Title = {A neurogenetics approach to understanding individual
             differences in brain, behavior, and risk for
             psychopathology},
   Journal = {Molecular Psychiatry},
   Volume = {18},
   Number = {3},
   Pages = {288-299},
   Address = {Laboratory of NeuroGenetics, Department of Psychology and
             Neuroscience, Duke University, Durham, NC 27705, USA.
             ryan.bogdan@duke.edu},
   Year = {2012},
   ISSN = {1359-4184},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/22614291},
   Abstract = {Neurogenetics research has begun to advance our
             understanding of how genetic variation gives rise to
             individual differences in brain function, which, in turn,
             shapes behavior and risk for psychopathology. Despite these
             advancements, neurogenetics research is currently confronted
             by three major challenges: (1) conducting research on
             individual variables with small effects, (2) absence of
             detailed mechanisms, and (3) a need to translate findings
             toward greater clinical relevance. In this review, we
             showcase techniques and developments that address these
             challenges and highlight the benefits of a neurogenetics
             approach to understanding brain, behavior and
             psychopathology. To address the challenge of small effects,
             we explore approaches including incorporating the
             environment, modeling epistatic relationships and using
             multilocus profiles. To address the challenge of mechanism,
             we explore how non-human animal research, epigenetics
             research and genome-wide association studies can inform our
             mechanistic understanding of behaviorally relevant brain
             function. Finally, to address the challenge of clinical
             relevance, we examine how neurogenetics research can
             identify novel therapeutic targets and for whom treatments
             work best. By addressing these challenges, neurogenetics
             research is poised to exponentially increase our
             understanding of how genetic variation interacts with the
             environment to shape the brain, behavior and risk for
             psychopathology.Molecular Psychiatry advance online
             publication, 22 May 2012; doi:10.1038/mp.2012.35.},
   Language = {eng},
   Doi = {10.1038/mp.2012.35},
   Key = {Bogdan2013}
}

@article{Brown2012,
   Author = {Brown, AA and Jensen, J and Nikolova, YS and Djurovic, S and Agartz, I and Server, A and Ferrell, RE and Manuck, SB and Mattingsdal, M and Melle,
             I and Hariri, AR and Frigessi, A and Andreassen, OA},
   Title = {Genetic variants affecting the neural processing of human
             facial expressions: Evidence using a genome-wide functional
             imaging approach},
   Journal = {Translational Psychiatry},
   Volume = {2},
   Pages = {e143},
   Address = {Division of Mental Health and Addiction, Institute of
             Clinical Medicine, University of Oslo, Oslo, Norway.
             andrew.brown@medisin.uio.no},
   Year = {2012},
   ISSN = {2158-3188},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/22828495},
   Keywords = {Adult • Brain Mapping • *Facial Expression •
             Female • Genetic Variation • Genome-Wide
             Association Study • Humans • Magnetic Resonance
             Imaging/methods • Male • Polymorphism, Single
             Nucleotide • Reproducibility of Results • Temporal
             Lobe/*physiopathology • Visual Perception/*genetics},
   Abstract = {Human faces present crucial visual information for social
             interaction. Specialized brain regions are involved in the
             perception of faces, with the fusiform face area (FFA) a key
             neuronal substrate. Face processing is genetically
             controlled, but by which specific genes is unknown. A
             genome-wide approach identified common single nucleotide
             polymorphisms (SNPs) associated with areas of increased
             brain activity in response to affective facial expressions,
             measured with functional magnetic resonance imaging. SNPs in
             20 genetic regions were linked with neural responses to
             negative facial expressions in a Norwegian sample (n246),
             which included patients with mental illness. Three genetic
             regions were linked with FFA activation in a further
             discovery experiment using positive facial expressions and
             involving many of the same individuals (n284). Two of these
             three regions showed significant association with right FFA
             activation to negative facial expressions in an independent
             North American replication sample of healthy Caucasians
             (n85, 3q26.31, P0.004; 20p12.3, P0.045). The activation
             patterns were particularly striking for the SNP in 3q26.31,
             which lies in a gene TMEM212; only the FFA was activated.
             The specialized function of this brain region suggests that
             TMEM212 could contribute to the innate architecture of face
             processing. © 2012 Macmillan Publishers Limited All rights
             reserved 2158-3188/12.},
   Language = {eng},
   Doi = {10.1038/tp.2012.67},
   Key = {Brown2012}
}

@article{Joeyen-Waldorf2012,
   Author = {Joeyen-Waldorf, J and Nikolova, YS and Edgar, N and Walsh, C and Kota,
             R and Lewis, DA and Ferrell, R and Manuck, SB and Hariri, AR and Sibille,
             E},
   Title = {Adenylate cyclase 7 is implicated in the biology of
             depression and modulation of affective neural
             circuitry},
   Journal = {Biological Psychiatry},
   Volume = {71},
   Number = {7},
   Pages = {627-632},
   Address = {Department of Psychiatry, University of Pittsburgh,
             Pennsylvania 15219, USA.},
   Year = {2012},
   ISSN = {0006-3223},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/22264442},
   Keywords = {Adenylate Cyclase/genetics/metabolism/*physiology •
             Adult • Amygdala/metabolism/*physiopathology •
             Animals • Depressive Disorder/genetics/metabolism/*physiopathology
             • Disease Models, Animal • Emotions/*physiology
             • Female • Functional Neuroimaging/methods/*psychology
             • Gene Expression/genetics/physiology • Genetic
             Predisposition to Disease • Genotype • Gyrus
             Cinguli/physiopathology • Humans • Magnetic
             Resonance Imaging/methods/psychology • Male • Mice
             • Mice, Inbred C57BL • Mice, Knockout •
             Polymorphism, Single Nucleotide • Serotonin Plasma
             Membrane Transport Proteins/genetics},
   Abstract = {Background: Evolutionarily conserved genes and their
             associated molecular pathways can serve as a translational
             bridge between human and mouse research, extending our
             understanding of biological pathways mediating individual
             differences in behavior and risk for psychopathology.
             Methods: Comparative gene array analysis in the amygdala and
             cingulate cortex between the serotonin transporter knockout
             mouse, a genetic animal model replicating features of human
             depression, and existing brain transcriptome data from
             postmortem tissue derived from clinically depressed humans
             was conducted to identify genes with similar changes across
             species (i.e., conserved) that may help explain risk of
             depressive-like phenotypes. Human neuroimaging analysis was
             then used to investigate the impact of a common
             single-nucleotide polymorphism (rs1064448) in a gene with
             identified conserved human-mouse changes, adenylate cyclase
             7 (ADCY7), on threat-associated amygdala reactivity in two
             large independent samples. Results: Comparative analysis
             identified genes with conserved transcript changes in
             amygdala (n = 29) and cingulate cortex (n = 19), both
             critically involved in the generation and regulation of
             emotion. Selected results were confirmed by real-time
             quantitative polymerase chain reaction, including
             upregulation in the amygdala of transcripts for ADCY7, a
             gene previously implicated in human depression and
             associated with altered emotional responsiveness in mouse
             models. Translating these results back to living healthy
             human subjects, we show that genetic variation (rs1064448)
             in ADCY7 biases threat-related amygdala reactivity.
             Conclusions: This converging cross-species evidence
             implicates ADCY7 in the modulation of mood regulatory neural
             mechanisms and, possibly, risk for and pathophysiology of
             depression, together supporting a continuous dimensional
             approach to major depressive disorder and other affective
             disorders. © 2012 Society of Biological
             Psychiatry.},
   Language = {eng},
   Doi = {10.1016/j.biopsych.2011.11.029},
   Key = {Joeyen-Waldorf2012}
}

@article{Bogdan2012a,
   Author = {Bogdan, R and Williamson, DE and Hariri, AR},
   Title = {Mineralocorticoid receptor Iso/Val (rs5522) genotype
             moderates the association between previous childhood
             emotional neglect and amygdala reactivity},
   Journal = {American Journal of Psychiatry},
   Volume = {169},
   Number = {5},
   Pages = {515-522},
   Address = {Laboratory of NeuroGenetics, Department of Psychology and
             Neuroscience, and Institute for Genome Sciences and Policy,
             Duke University, Durham, NC, USA. bogdan.ryan@gmail.com},
   Year = {2012},
   ISSN = {0002-953X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/22407082},
   Keywords = {Adolescent • Alleles • Amygdala/*physiopathology
             • Child • *Child Abuse/psychology • Female
             • Functional Neuroimaging • Genotype •
             Homozygote • Humans • Magnetic Resonance Imaging
             • Male • Mutation, Missense/*genetics/physiology
             • Receptors, Mineralocorticoid/*genetics/physiology},
   Abstract = {Objective: The amygdala is especially reactive to
             threatening stimuli, and the degree of reactivity predicts
             individual differences in the expression of depression and
             anxiety. Emerging research suggests that emotional neglect
             during childhood as well as hypercortisolemia may lead to
             heightened threat-related amygdala reactivity. This raises
             the possibility that genetic variation affecting
             hypothalamic-pituitary-adrenal (HPA) axis function
             contributes to individual differences in amygdala
             reactivity, both independently and as a function of
             childhood emotional neglect. Method: This study assessed
             whether the mineralocorticoid receptor iso/val polymorphism
             (rs5522), a functional genetic variant affecting HPA axis
             function, influenced threat-related amygdala reactivity in
             279 individuals in late childhood and early adolescence. The
             study also explored the extent to which any effects of the
             genotype on amygdala reactivity were contingent upon
             previous childhood emotional neglect. Results: Prior
             childhood emotional neglect and the val allele were
             associated with greater amygdala reactivity. Moreover, a
             significant genotype-by-emotional neglect interaction was
             observed whereby greater amygdala reactivity in val allele
             carriers was independent of previous childhood emotional
             neglect, while greater reactivity in iso homozygotes was
             revealed only in the context of a history of elevated
             emotional neglect. At relatively low levels of previous
             emotional neglect, val carriers had heightened amygdala
             reactivity relative to iso homozygotes. Conclusions: These
             results suggest that relatively greater amygdala reactivity
             may represent a biological mechanism through which childhood
             adversity and functional genetic variation in HPA axis
             responsiveness to stress may mediate risk for
             psychopathology.},
   Language = {eng},
   Doi = {10.1176/appi.ajp.2011.11060855},
   Key = {Bogdan2012a}
}

@article{Lahey2012a,
   Author = {Lahey, BB and McNealy, K and Knodt, A and Zald, DH and Sporns, O and Manuck, SB and Flory, JD and Applegate, B and Rathouz, PJ and Hariri,
             AR},
   Title = {Using confirmatory factor analysis to measure
             contemporaneous activation of defined neuronal networks in
             functional magnetic resonance imaging},
   Journal = {NeuroImage},
   Volume = {60},
   Number = {4},
   Pages = {1982-1991},
   Address = {Department of Health Studies, University of Chicago,
             Chicago, IL 60637, United States. blahey@health.bsd.uchicago.edu},
   Year = {2012},
   ISSN = {1053-8119},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/22348884},
   Keywords = {Adolescent • Adult • Brain/physiology • Brain
             Mapping/*methods • *Factor Analysis, Statistical •
             Female • Humans • Image Interpretation,
             Computer-Assisted/*methods • *Magnetic Resonance
             Imaging • Male • *Models, Theoretical • Young
             Adult},
   Abstract = {Functional neuroimaging often generates large amounts of
             data on regions of interest. Such data can be addressed
             effectively with a widely-used statistical technique based
             on measurement theory that has not yet been applied to
             neuroimaging. Confirmatory factor analysis is a convenient
             hypothesis-driven modeling environment that can be used to
             conduct formal statistical tests comparing alternative
             hypotheses regarding the elements of putative neuronal
             networks. In such models, measures of each activated region
             of interest are treated as indicators of an underlying
             latent construct that represents the contemporaneous
             activation of the elements in the network. As such,
             confirmatory factor analysis focuses analyses on the
             activation of hypothesized networks as a whole, improves
             statistical power by modeling measurement error, and
             provides a theory-based approach to data reduction with a
             robust statistical basis. This approach is illustrated using
             data on seven regions of interest in a hypothesized
             mesocorticostriatal reward system in a sample of 262 adult
             volunteers assessed during a card-guessing reward task. A
             latent construct reflecting contemporaneous activation of
             the reward system was found to be significantly associated
             with a latent construct measuring impulsivity, particularly
             in males. © 2012 Elsevier Inc..},
   Language = {eng},
   Doi = {10.1016/j.neuroimage.2012.02.002},
   Key = {Lahey2012a}
}

@article{Terburg2012,
   Author = {Terburg, D and Morgan, BE and Montoya, ER and Hooge, IT and Thornton,
             HB and Hariri, AR and Panksepp, J and Stein, DJ and Honk,
             JV},
   Title = {Hypervigilance for fear after basolateral amygdala damage in
             humans},
   Journal = {Translational Psychiatry},
   Volume = {2},
   Pages = {e115},
   Address = {Department of Psychology, Utrecht University, Utrecht, The
             Netherlands. d.terburg@uu.nl},
   Year = {2012},
   ISSN = {2158-3188},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/22832959},
   Keywords = {Adult • Amygdala/*physiopathology •
             Anxiety/genetics/pathology/*physiopathology • Attention
             • Brain Damage, Chronic/genetics/pathology/*physiopathology
             • Brain Mapping • Calcinosis/genetics/pathology/physiopathology
             • Discrimination (Psychology)/physiology •
             Dominance, Cerebral/physiology • Emotions/physiology
             • Facial Expression • Fear/*physiology •
             Female • Humans • Image Interpretation,
             Computer-Assisted • Lipoid Proteinosis of Urbach and
             Wiethe/genetics/pathology/*physiopathology • Magnetic
             Resonance Imaging • Male • Middle Aged •
             Nerve Growth Factors • Neural Inhibition/*physiology
             • Pattern Recognition, Visual/physiology •
             Recognition (Psychology)/physiology • Reference Values
             • Stroop Test • Subliminal Stimulation},
   Abstract = {Recent rodent research has shown that the basolateral
             amygdala (BLA) inhibits unconditioned, or innate, fear. It
             is, however, unknown whether the BLA acts in similar ways in
             humans. In a group of five subjects with a rare genetic
             syndrome, that is, Urbach-Wiethe disease (UWD), we used a
             combination of structural and functional neuroimaging, and
             established focal, bilateral BLA damage, while other
             amygdala sub-regions are functionally intact. We tested the
             translational hypothesis that these BLA-damaged UWD-subjects
             are hypervigilant to facial expressions of fear, which are
             prototypical innate threat cues in humans. Our data indeed
             repeatedly confirm fear hypervigilance in these UWD
             subjects. They show hypervigilant responses to unconsciously
             presented fearful faces in a modified Stroop task. They
             attend longer to the eyes of dynamically displayed fearful
             faces in an eye-tracked emotion recognition task, and in
             that task recognize facial fear significantly better than
             control subjects. These findings provide the first direct
             evidence in humans in support of an inhibitory function of
             the BLA on the brain's threat vigilance system, which has
             important implications for the understanding of the
             amygdala's role in the disorders of fear and anxiety. ©
             2012 Macmillan Publishers Limited All rights
             reserved.},
   Language = {eng},
   Doi = {10.1038/tp.2012.46},
   Key = {Terburg2012}
}

@article{White2012,
   Author = {White, MG and Bogdan, R and Fisher, PM and Muñoz, KE and Williamson,
             DE and Hariri, AR},
   Title = {FKBP5 and emotional neglect interact to predict individual
             differences in amygdala reactivity},
   Journal = {Genes, Brain and Behavior},
   Volume = {11},
   Number = {7},
   Pages = {869-878},
   Address = {Laboratory of NeuroGenetics, Department of Psychology \&
             Neuroscience, Duke University, Durham, NC,
             USA.},
   Year = {2012},
   ISSN = {1601-1848},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/22979952},
   Keywords = {Adolescent • Alleles • Amygdala/pathology/*physiopathology
             • *Child Abuse • Female • Gene-Environment
             Interaction • Haplotypes • Humans • Magnetic
             Resonance Imaging • Polymorphism, Single Nucleotide
             • Risk Factors • Stress, Psychological/pathology
             • Tacrolimus Binding Proteins/*genetics},
   Abstract = {FKBP5 SNPs showing significant interaction effects with
             emotional neglect on right dorsal amygdala reactivity.
             Individual variation in physiological responsiveness to
             stress mediates risk for mental illness and is influenced by
             both experiential and genetic factors. Common polymorphisms
             in the human gene for FK506 binding protein 5 (FKBP5), which
             is involved in transcriptional regulation of the
             hypothalamic-pituitary-adrenal (HPA) axis, have been shown
             to interact with childhood abuse and trauma to predict
             stress-related psychopathology. In the current study, we
             examined if such gene-environment interaction effects may be
             related to variability in the threat-related reactivity of
             the amygdala, which plays a critical role in mediating
             physiological and behavioral adaptations to stress including
             modulation of the HPA axis. To this end, 139 healthy
             Caucasian youth completed a blood oxygen level-dependent
             functional magnetic resonance imaging probe of amygdala
             reactivity and self-report assessments of emotional neglect
             (EN) and other forms of maltreatment. These individuals were
             genotyped for 6 FKBP5 polymorphisms (rs7748266, rs1360780,
             rs9296158, rs3800373, rs9470080 and rs9394309) previously
             associated with psychopathology and/or HPA axis function.
             Interactions between each SNP and EN emerged such that risk
             alleles predicted relatively increased dorsal amygdala
             reactivity in the context of higher EN, even after
             correcting for multiple testing. Two different haplotype
             analyses confirmed this relationship as haplotypes with risk
             alleles also exhibited increased amygdala reactivity in the
             context of higher EN. Our results suggest that increased
             threat-related amygdala reactivity may represent a mechanism
             linking psychopathology to interactions between common
             genetic variants affecting HPA axis function and childhood
             trauma. © 2012 Blackwell Publishing Ltd and International
             Behavioural and Neural Genetics Society.},
   Language = {eng},
   Doi = {10.1111/j.1601-183X.2012.00837.x},
   Key = {White2012}
}

@article{Bogdan2012c,
   Author = {Bogdan, R and Carre, JM and Hariri, AR},
   Title = {Toward a mechanistic understanding of how variability in
             neurobiology shapes individual differences in
             behavior},
   Journal = {Current topics in behavioral neurosciences},
   Volume = {12},
   Pages = {361-393},
   Address = {Laboratory of NeuroGenetics, Department of Psychology \&
             Neuroscience, Institute for Genome Sciences \& Policy, Duke
             University, 417 Chapel Drive, Durham, NC, 27708, USA,
             bogdan.ryan@gmail.com.},
   Year = {2012},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/22437943},
   Abstract = {Research has begun to identify how variability in brain
             function contributes to individual differences in complex
             behavioral traits. Examining variability in molecular
             signaling pathways with emerging and established
             methodologies such as pharmacologic fMRI, multimodal
             PET/fMRI, and hormonal assays are beginning to provide a
             mechanistic understanding of how individual differences in
             brain function arise. Against this background, functional
             genetic polymorphisms are being utilized to understand the
             origins of variability in signaling pathways as well as to
             efficiently model how such emergent variability impacts
             behaviorally relevant brain function and health outcomes.
             This chapter provides an overview of a research strategy
             that integrates these complimentary levels of analysis;
             existing empirical data is used to illustrate the
             effectiveness of this approach in illuminating the
             mechanistic neurobiology of individual differences in
             complex behavioral traits. This chapter also discusses how
             such efforts can contribute to the identification of
             predictive risk markers that interact with unique
             environmental factors to precipitate psychopathology.},
   Language = {eng},
   Doi = {10.1007/7854_2011_182},
   Key = {Bogdan2012c}
}

@article{Hariri2012,
   Author = {Hariri, AR},
   Title = {The highs and lows of amygdala reactivity in bipolar
             disorders},
   Journal = {American Journal of Psychiatry},
   Volume = {169},
   Number = {8},
   Pages = {780-783},
   Year = {2012},
   ISSN = {0002-953X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/22854927},
   Keywords = {Bipolar Disorder/*physiopathology •
             Brain/*physiopathology • Emotions/*physiology •
             Female • Humans • *Magnetic Resonance Imaging
             • Male},
   Language = {eng},
   Doi = {10.1176/appi.ajp.2012.12050639},
   Key = {Hariri2012}
}

@article{Minkel2012,
   Author = {Minkel, JD and McNealy, K and Gianaros, PJ and Drabant, EM and Gross,
             JJ and Manuck, SB and Hariri, AR},
   Title = {Sleep quality and neural circuit function supporting emotion
             regulation},
   Journal = {Biology of mood \& anxiety disorders},
   Volume = {2},
   Number = {1},
   Pages = {22},
   Address = {Laboratory of NeuroGenetics, Department of Psychology \&
             Neuroscience, Duke University, 417 Chapel Dr,, Durham, NC
             27708, USA. jared.minkel@duke.edu.},
   Year = {2012},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/23216889},
   Abstract = {ABSTRACT: BACKGROUND: Recent laboratory studies employing an
             extended sleep deprivation model have mapped sleep-related
             changes in behavior onto functional alterations in specific
             brain regions supporting emotion, suggesting possible
             biological mechanisms for an association between sleep
             difficulties and deficits in emotion regulation. However, it
             is not yet known if similar behavioral and neural changes
             are associated with the more modest variability in sleep
             observed in daily life. METHODS: We examined relationships
             between sleep and neural circuitry of emotion using the
             Pittsburgh Sleep Quality Index and fMRI data from a widely
             used emotion regulation task focusing on cognitive
             reappraisal of negative emotional stimuli in an unselected
             sample of 97 adult volunteers (48 women; mean age
             42.78+/-7.37years, range 30--54years old). RESULTS: Emotion
             regulation was associated with greater activation in
             clusters located in the dorsomedial prefrontal cortex
             (dmPFC), left dorsolateral prefrontal cortex (dlPFC), and
             inferior parietal cortex. Only one subscale from the
             Pittsburgh Sleep Quality Index, use of sleep medications,
             was related to BOLD responses in the dmPFC and dlPFC during
             cognitive reappraisal. Use of sleep medications predicted
             lesser BOLD responses during reappraisal, but other aspects
             of sleep, including sleep duration and subjective sleep
             quality, were not related to neural activation in this
             paradigm. CONCLUSIONS: The relatively modest variability in
             sleep that is common in the general community is unlikely to
             cause significant disruption in neural circuits supporting
             reactivity or regulation by cognitive reappraisal of
             negative emotion. Use of sleep medication however, may
             influence emotion regulation circuitry, but additional
             studies are necessary to determine if such use plays a
             causal role in altering emotional responses.},
   Language = {eng},
   Doi = {10.1186/2045-5380-2-22},
   Key = {Minkel2012}
}

@article{Bogdan2012b,
   Author = {Bogdan, R and Hariri, AR},
   Title = {Neural embedding of stress reactivity},
   Journal = {Nature Neuroscience},
   Volume = {15},
   Number = {12},
   Pages = {1605-1607},
   Year = {2012},
   ISSN = {1097-6256},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/23187689},
   Keywords = {Adolescent Behavior/*physiology • Amygdala/*growth \&
             development • Anxiety/*metabolism •
             Depression/*metabolism • Female • Humans •
             Hydrocortisone/*metabolism • Male • Prefrontal
             Cortex/*growth \& development},
   Language = {eng},
   Doi = {10.1038/nn.3270},
   Key = {Bogdan2012b}
}

@article{Carre2012,
   Author = {Carré, JM and Fisher, PM and Manuck, SB and Hariri,
             AR},
   Title = {Interaction between trait anxiety and trait anger predict
             amygdala reactivity to angry facial expressions in men but
             not women},
   Journal = {Social Cognitive and Affective Neuroscience},
   Volume = {7},
   Number = {2},
   Pages = {213-221},
   Address = {Department of Psychology and Neuroscience, Duke University,
             Durham, NC 27708, USA. justin.carre@duke.edu},
   Year = {2012},
   ISSN = {1749-5016},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/21183456},
   Keywords = {Adult • Amygdala/*physiology • Anger/*physiology
             • Anxiety/*psychology • Brain/physiology •
             Emotions/physiology • *Facial Expression • Female
             • Humans • Individuality • Male • Middle
             Aged • Neuroimaging},
   Abstract = {The amygdala is critically involved in mediating
             physiological and behavioral responses to threat. In
             particular, neuroimaging research indicates that the
             amygdala is highly responsive to facial signals of threat
             such as fearful and angry expressions. However, individuals
             differ substantially in both their relative sensitivity to
             threat and the magnitude of amygdala reactivity to facial
             signals of threat. Here, we report the novel finding that
             individual differences in trait anger are positively
             correlated with bilateral dorsal amygdala reactivity to
             angry facial expressions, but only among men with elevated
             trait anxiety scores. These findings add to the growing body
             of evidence indicating that variability in personality
             traits contribute to individual differences in
             threat-related amygdala reactivity and further suggest that
             heightened amygdala reactivity to angry faces may be
             uniquely involved in the expression of reactive aggression
             in men. © The Author (2010). Published by Oxford University
             Press.},
   Language = {eng},
   Doi = {10.1093/scan/nsq101},
   Key = {Carre2012}
}

@article{Carre2013b,
   Author = {Carre, JM and Hyde, LW and Neumann, CS and Viding, E and Hariri,
             AR},
   Title = {The neural signatures of distinct psychopathic
             traits},
   Journal = {Social neuroscience},
   Volume = {8},
   Number = {2},
   Pages = {122--35},
   Address = {Laboratory of NeuroGenetics, Department of Psychology and
             Neuroscience, Duke University, Durham, NC, USA.
             justin.carre@wayne.edu},
   Year = {2012},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/22775289},
   Keywords = {Amygdala/pathology • Antisocial Personality
             Disorder/pathology/psychology • Data Interpretation,
             Statistical • Female • Humans • Image
             Processing, Computer-Assisted • Impulsive
             Behavior/pathology/psychology • Magnetic Resonance
             Imaging • Male • Neostriatum/pathology •
             Nervous System/*pathology • Neuropsychological Tests
             • Oxygen/blood • Reward • Sex Characteristics
             • Young Adult},
   Abstract = {Recent studies suggest that psychopathy may be associated
             with dysfunction in the neural circuitry supporting both
             threat- and reward-related processes. However, these studies
             have involved small samples and often focused on extreme
             groups. Thus, it is unclear to what extent current findings
             may generalize to psychopathic traits in the general
             population. Furthermore, no studies have systematically and
             simultaneously assessed associations between distinct
             psychopathy facets and both threat- and reward-related brain
             function in the same sample of participants. Here, we
             examined the relationship between threat-related amygdala
             reactivity and reward-related ventral striatum (VS)
             reactivity and variation in four facets of self-reported
             psychopathy in a sample of 200 young adults. Path models
             indicated that amygdala reactivity to fearful facial
             expressions is negatively associated with the interpersonal
             facet of psychopathy, whereas amygdala reactivity to angry
             facial expressions is positively associated with the
             lifestyle facet. Furthermore, these models revealed that
             differential VS reactivity to positive versus negative
             feedback is negatively associated with the lifestyle facet.
             There was suggestive evidence for gender-specific patterns
             of association between brain function and psychopathy
             facets. Our findings are the first to document differential
             associations between both threat- and reward-related neural
             processes and distinct facets of psychopathy and thus
             provide a more comprehensive picture of the pattern of
             neural vulnerabilities that may predispose to maladaptive
             outcomes associated with psychopathy.},
   Language = {eng},
   Doi = {10.1080/17470919.2012.703623},
   Key = {Carre2013b}
}

@article{Ousdal2012,
   Author = {Ousdal, OT and Brown, AA and Jensen, J and Nakstad, PH and Melle, I and Agartz, I and Djurovic, S and Bogdan, R and Hariri, AR and Andreassen,
             OA},
   Title = {Associations between variants near a monoaminergic pathways
             gene (PHOX2B) and amygdala reactivity: A genome-wide
             functional imaging study},
   Journal = {Twin Research & Human Genetics},
   Volume = {15},
   Number = {3},
   Pages = {273-285},
   Address = {Oslo University Hospital, Oslo, Norway. o.t.ousdal@medisin.uio.no},
   Year = {2012},
   ISSN = {1832-4274},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/22856363},
   Keywords = {Adult • Amygdala/*physiology • Bipolar
             Disorder/genetics/physiopathology •
             Catecholamines/biosynthesis • Female •
             *Genome-Wide Association Study • Genotype •
             Homeodomain Proteins/*genetics/metabolism • Humans
             • Linkage Disequilibrium • *Magnetic Resonance
             Imaging • Male • *Polymorphism, Single Nucleotide
             • Schizophrenia/genetics/physiopathology •
             Serotonin/biosynthesis • Signal Transduction/*genetics
             • Transcription Factors/*genetics/metabolism},
   Abstract = {As the amygdala is part of the phylogenetic old brain, and
             its anatomical and functional properties are conserved
             across species, it is reasonable to assume genetic influence
             on its activity. A large corpus of candidate gene studies
             indicate that individual differences in amygdala activity
             may be caused by genetic variants within monoaminergic
             signaling pathways such as dopamine, serotonin, and
             norepinephrine. However, to our knowledge, the use of
             genome-wide data to discover genetic variants underlying
             individual differences in adult amygdala activity is novel.
             In the present study, the combination of genome-wide data
             and functional imaging phenotypes from an emotional faces
             task yielded a significant association between rs10014254
             and the amygdala using a region of interest approach. This
             single nucleotide polymorphism is located in a regulatory
             region upstream of the Paired-like homeobox 2b (PHOX2B)
             gene; therefore it could affect the expression of this gene.
             PHOX2B regulates the expression of enzymes necessary for the
             synthesis of several monoamines and is essential for the
             development of the autonomic nervous system. However, an
             attempt to replicate the finding in an independent sample
             from North America did not succeed. The synthesis of
             functional magnetic resonance imaging (fMRI) and genome-wide
             data takes a hypothesis-free approach as to which genetic
             variants are of interest. Therefore, we believe that an
             undirected finding within such a plausible region is of
             interest, and that our results add further support to the
             hypothesis that monoaminergic signaling pathways play a
             central role in regulating amygdala activity. © The Authors
             2012.},
   Language = {eng},
   Doi = {10.1017/thg.2012.5},
   Key = {Ousdal2012}
}

@article{Nikolova2012a,
   Author = {Nikolova, YS and Hariri, AR},
   Title = {Neural responses to threat and reward interact to predict
             stress-related problem drinking: A novel protective role of
             the amygdala},
   Journal = {Biology of mood \& anxiety disorders},
   Volume = {2},
   Number = {1},
   Pages = {19},
   Address = {Laboratory of NeuroGenetics, Department of Psychology \&
             Neuroscience and Institute for Genome Sciences \& Policy,
             Duke University, NC 27708, Durham, USA. yuliya.nikolova@duke.edu.},
   Year = {2012},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/23151390},
   Abstract = {ABSTRACT: BACKGROUND: Research into neural mechanisms of
             drug abuse risk has focused on the role of dysfunction in
             neural circuits for reward. In contrast, few studies have
             examined the role of dysfunction in neural circuits of
             threat in mediating drug abuse risk. Although typically
             regarded as a risk factor for mood and anxiety disorders,
             threat-related amygdala reactivity may serve as a protective
             factor against substance use disorders, particularly in
             individuals with exaggerated responsiveness to reward.
             FINDINGS: We used well-established neuroimaging paradigms to
             probe threat-related amygdala and reward-related ventral
             striatum reactivity in a sample of 200 young adult students
             from the ongoing Duke Neurogenetics Study. Recent life
             stress and problem drinking were assessed using self-report.
             We found a significant three-way interaction between
             threat-related amygdala reactivity, reward-related ventral
             striatum reactivity, and recent stress, wherein individuals
             with higher reward-related ventral striatum reactivity
             exhibit higher levels of problem drinking in the context of
             stress, but only if they also have lower threat-related
             amygdala reactivity. This three-way interaction predicted
             both contemporaneous problem drinking and problem drinking
             reported three-months later in a subset of participants.
             CONCLUSIONS: These findings suggest complex interactions
             between stress and neural responsiveness to both threat and
             reward mediate problem drinking. Furthermore, they highlight
             a novel protective role for threat-related amygdala
             reactivity against drug use in individuals with high neural
             reactivity to reward.},
   Language = {eng},
   Doi = {10.1186/2045-5380-2-19},
   Key = {Nikolova2012a}
}

@article{Josephs2012,
   Author = {Josephs, RA and Telch, MJ and Hixon, JG and Evans, JJ and Lee, H and Knopik, VS and McGeary, JE and Hariri, AR and Beevers,
             CG},
   Title = {Genetic and hormonal sensitivity to threat: Testing a
             serotonin transporter genotype×testosterone
             interaction},
   Journal = {Psychoneuroendocrinology},
   Volume = {37},
   Number = {6},
   Pages = {752-761},
   Address = {Department of Psychology, The University of Texas at Austin,
             Austin, TX 78756, USA. josephs@mail.psy.utexas.edu},
   Year = {2012},
   ISSN = {0306-4530},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/21978869},
   Keywords = {Carbon Dioxide/diagnostic use • DNA/genetics •
             Depression/genetics/psychology • Ethnic Groups •
             Female • Genotype • Heterozygote • Humans
             • Hydrocortisone/blood • Male • Military
             Personnel • Psychiatric Status Rating Scales •
             Psychomotor Performance/physiology • Questionnaires
             • Saliva/chemistry • Serotonin Plasma Membrane
             Transport Proteins/*genetics/*metabolism • Social
             Environment • Stress, Psychological/*genetics/*metabolism
             • Testosterone/*blood • Young Adult},
   Abstract = {Background: Striking parallels are observed when comparing
             the literature on the 5-HTTLPR of the serotonin transporter
             gene (SLC6A4) to the testosterone (T) literature on measures
             of stress reactivity and neural activity. Short (S) allele
             carriers and individuals higher in testosterone levels show
             exaggerated stress responses, amygdala hyperactivity, and
             reduction of amygdala-prefrontal cortex coupling when
             exposed to threat. Methods: Three studies tested the
             hypothesis that higher T, S carriers would show increased
             cortisol responses to threat. Results: Supporting the
             hypothesis, a T × 5-HTTLPR interaction was obtained across
             all studies. Threats to status via social exclusion (Study
             1), cognitive/perceptual failure (Study 2), and physical
             competence (Study 3) all produced elevated cortisol levels
             in S carriers with higher T levels. An unexpected result was
             that 5-HTTLPR long (L) allele homozygotes with higher T
             showed lower cortisol levels in response to threat-a pattern
             of response that closely parallels that reported for
             psychopathic individuals. Finally, combining effect sizes
             across studies showed that the likelihood that these effects
             were due to Type 1 errors was quite low. Conclusions: What
             emerges from these studies is a novel yet reliable, and
             synergistic relationship between 5-HTTLPR genotype and
             testosterone on stress reactivity, possibly conferring
             vulnerability for multiple neuropsychiatric disorders. ©
             2011 Elsevier Ltd.},
   Language = {eng},
   Doi = {10.1016/j.psyneuen.2011.09.006},
   Key = {Josephs2012}
}

@article{Lahey2012b,
   Author = {Lahey, BB and Applegate, B and Hakes, JK and Zald, DH and Hariri, AR and Rathouz, PJ},
   Title = {Is there a general factor of prevalent psychopathology
             during adulthood?},
   Journal = {Journal of abnormal psychology},
   Volume = {121},
   Number = {4},
   Pages = {971-977},
   Address = {Department of Health Studies (MC 2007), University of
             Chicago, Chicago, IL 60637, USA. blahey@uchicago.edu},
   Year = {2012},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/22845652},
   Keywords = {Adolescent • Adult • Comorbidity • Diagnostic
             and Statistical Manual of Mental Disorders • Factor
             Analysis, Statistical • Female • Humans •
             Interview, Psychological • Male • Mental
             Disorders/diagnosis/*epidemiology • Middle Aged •
             *Models, Psychological • Prevalence},
   Abstract = {The patterns of comorbidity among prevalent mental disorders
             in adults lead them to load on ``externalizing,''
             ``distress,'' and ``fears'' factors. These factors are
             themselves robustly correlated, but little attention has
             been paid to this fact. As a first step in studying the
             implications of these interfactor correlations, we conducted
             confirmatory factor analyses on diagnoses of 11 prevalent
             Diagnostic and Statistical Manual of Mental Disorders (4th
             ed.) mental disorders in a nationally representative sample.
             A model specifying correlated externalizing, distress, and
             fears factors fit well, but an alternative model was tested
             in which a ``general'' bifactor was added to capture what
             these disorders share in common. There was a modest but
             significant improvement in fit for the bifactor model
             relative to the 3-factor oblique model, with all disorders
             loading strongly on the bifactor. Tests of external validity
             revealed that the fears, distress, and externalizing factors
             were differentially associated with measures of functioning
             and potential risk factors. Nonetheless, the general
             bifactor accounted for significant independent variance in
             future psychopathology, functioning, and other criteria over
             and above the fears, distress, and externalizing factors.
             These findings support the hypothesis that these prevalent
             forms of psychopathology have both important common and
             unique features. Future studies should determine whether
             this is because they share elements of their etiology and
             neurobiological mechanisms. If so, the existence of common
             features across diverse forms of prevalent psychopathology
             could have important implications for understanding the
             nature, etiology, and outcomes of psychopathology. (PsycINFO
             Database Record (c) 2012 APA, all rights
             reserved).},
   Language = {eng},
   Doi = {10.1037/a0028355},
   Key = {Lahey2012b}
}

@article{Drabant2012,
   Author = {Drabant, EM and Ramel, W and Edge, MD and Hyde, LW and Kuo, JR and Goldin,
             PR and Hariri, AR and Gross, JJ},
   Title = {Neural mechanisms underlying 5-HTTLPR-related sensitivity to
             acute stress},
   Journal = {American Journal of Psychiatry},
   Volume = {169},
   Number = {4},
   Pages = {397-405},
   Address = {Department of Psychology, Stanford University, Stanford,
             California, USA.},
   Year = {2012},
   ISSN = {0002-953X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/22362395},
   Keywords = {Adult • Alleles • Brain/*physiopathology •
             Female • Functional Neuroimaging/methods/*psychology
             • Genotype • Humans • Magnetic Resonance
             Imaging/methods/*psychology • Neural
             Pathways/physiopathology • Polymorphism, Single
             Nucleotide • Serotonin Plasma Membrane Transport
             Proteins/genetics/*physiology • Stress,
             Psychological/genetics/*physiopathology},
   Abstract = {Objective: Many studies have shown that 5-HTTLPR genotype
             interacts with exposure to stress in conferring risk for
             psychopathology. However, the specific neural mechanisms
             through which this gene-by- environment interaction confers
             risk remain largely unknown, and no study to date has
             directly examined the modulatory effects of 5-HTTLPR on
             corticolimbic circuit responses during exposure to acute
             stress. Method: An acute laboratory stressor was
             administered to 51 healthy women during blood-oxygen-level-dependent
             functional magnetic resonance imaging. In this task,
             participants were threatened with electric shocks of
             uncertain intensity, which were unpredictably delivered to
             the wrist after a long anticipatory cue period of
             unpredictable duration. Results: Relative to women carrying
             the L allele, those with the SS genotype showed enhanced
             activation during threat anticipation in a network of
             regions, including the amygdala, hippocampus, anterior
             insula, thalamus, pulvinar, caudate, precuneus, anterior
             cingulate cortex, and medial prefrontal cortex. Individuals
             with the SS genotype also displayed enhanced positive
             coupling between medial prefrontal cortex activation and
             anxiety experience, whereas enhanced negative coupling
             between insula activation and perceived success at
             regulating anxiety was observed in individuals carrying the
             L allele. Conclusions: These findings suggest that during
             stress exposure, neural systems that enhance fear and
             arousal, modulate attention toward threat, and perseverate
             on emotional salience of the threat may be engaged
             preferentially in individuals with the SS genotype. This may
             be one mechanism underlying the risk for psychopathology
             conferred by the S allele upon exposure to life
             stressors.},
   Language = {eng},
   Doi = {10.1176/appi.ajp.2011.10111699},
   Key = {Drabant2012}
}

@article{Morey2011,
   Author = {Morey, RA and Hariri, AR and Gold, AL and Hauser, MA and Munger, HJ and Dolcos, F and McCarthy, G},
   Title = {Serotonin transporter gene polymorphisms and brain function
             during emotional distraction from cognitive processing in
             posttraumatic stress disorder.},
   Journal = {BMC Psychiatry},
   Volume = {11},
   Pages = {76},
   Address = {Department of Psychiatry and Behavioral Sciences, Duke
             University, Durham, NC 27710, USA. morey@biac.duke.edu},
   Year = {2011},
   Month = {May},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/21545724},
   Keywords = {Amygdala/physiopathology • Case-Control Studies •
             Cognition/*physiology • Emotions/*physiology •
             Functional Neuroimaging/methods/psychology • Humans
             • Magnetic Resonance Imaging/psychology • Memory,
             Short-Term/physiology • *Polymorphism, Single
             Nucleotide • Prefrontal Cortex/physiopathology •
             Promoter Regions, Genetic/genetics/physiology •
             Psychomotor Performance/physiology • September 11
             Terrorist Attacks/psychology • Serotonin Plasma
             Membrane Transport Proteins/genetics/*physiology •
             Stress Disorders, Post-Traumatic/*genetics/*physiopathology/psychology
             • Veterans/psychology • Wounds and
             Injuries/physiopathology/psychology},
   Abstract = {BACKGROUND: Serotonergic system dysfunction has been
             implicated in posttraumatic stress disorder (PTSD). Genetic
             polymorphisms associated with serotonin signaling may
             predict differences in brain circuitry involved in emotion
             processing and deficits associated with PTSD. In healthy
             individuals, common functional polymorphisms in the
             serotonin transporter gene (SLC6A4) have been shown to
             modulate amygdala and prefrontal cortex (PFC) activity in
             response to salient emotional stimuli. Similar patterns of
             differential neural responses to emotional stimuli have been
             demonstrated in PTSD but genetic factors influencing these
             activations have yet to be examined. METHODS: We
             investigated whether SLC6A4 promoter polymorphisms
             (5-HTTLPR, rs25531) and several downstream single nucleotide
             polymorphisms (SNPs) modulated activity of brain regions
             involved in the cognitive control of emotion in post-9/11
             veterans with PTSD. We used functional MRI to examine neural
             activity in a PTSD group (n = 22) and a trauma-exposed
             control group (n = 20) in response to trauma-related images
             presented as task-irrelevant distractors during the active
             maintenance period of a delayed-response working memory
             task. Regions of interest were derived by contrasting
             activation for the most distracting and least distracting
             conditions across participants. RESULTS: In patients with
             PTSD, when compared to trauma-exposed controls, rs16965628
             (associated with serotonin transporter gene expression)
             modulated task-related ventrolateral PFC activation and
             5-HTTLPR tended to modulate left amygdala activation.
             Subsequent to combat-related trauma, these SLC6A4
             polymorphisms may bias serotonin signaling and the neural
             circuitry mediating cognitive control of emotion in patients
             with PTSD. CONCLUSIONS: The SLC6A4 SNP rs16965628 and
             5-HTTLPR are associated with a bias in neural responses to
             traumatic reminders and cognitive control of emotions in
             patients with PTSD. Functional MRI may help identify
             intermediate phenotypes and dimensions of PTSD that clarify
             the functional link between genes and disease phenotype, and
             also highlight features of PTSD that show more proximal
             influence of susceptibility genes compared to current
             clinical categorizations.},
   Language = {eng},
   Doi = {10.1186/1471-244X-11-76},
   Key = {Morey2011}
}

@article{Gianaros2011,
   Author = {Gianaros, PJ and Manuck, SB and Sheu, LK and Kuan, DCH and Votruba-Drzal, E and Craig, AE and Hariri, AR},
   Title = {Parental education predicts corticostriatal functionality in
             adulthood.},
   Journal = {Cerebral Cortex},
   Volume = {21},
   Number = {4},
   Pages = {896-910},
   Address = {Department of Psychiatry, University of Pittsburgh,
             Pittsburgh, PA 15213, USA. gianarospj@upmc.edu},
   Year = {2011},
   Month = {April},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/20810623},
   Keywords = {Adult • Cerebral Cortex/*physiology • *Educational
             Status • Female • Humans • Magnetic Resonance
             Imaging • Male • Middle Aged • Neural
             Pathways/*physiology • *Parents • Socioeconomic
             Factors},
   Abstract = {Socioeconomic disadvantage experienced in early development
             predicts ill health in adulthood. However, the
             neurobiological pathways linking early disadvantage to adult
             health remain unclear. Lower parental education-a
             presumptive indicator of early socioeconomic
             disadvantage-predicts health-impairing adult behaviors,
             including tobacco and alcohol dependencies. These behaviors
             depend, in part, on the functionality of corticostriatal
             brain systems that 1) show developmental plasticity and
             early vulnerability, 2) process reward-related information,
             and 3) regulate impulsive decisions and actions. Hence,
             corticostriatal functionality in adulthood may covary
             directly with indicators of early socioeconomic
             disadvantage, particularly lower parental education. Here,
             we tested the covariation between parental education and
             corticostriatal activation and connectivity in 76 adults
             without confounding clinical syndromes. Corticostriatal
             activation and connectivity were assessed during the
             processing of stimuli signaling monetary gains (positive
             feedback [PF]) and losses (negative feedback). After
             accounting for participants' own education and other
             explanatory factors, lower parental education predicted
             reduced activation in anterior cingulate and dorsomedial
             prefrontal cortices during PF, along with reduced
             connectivity between these cortices and orbitofrontal and
             striatal areas implicated in reward processing and impulse
             regulation. In speculation, adult alterations in
             corticostriatal functionality may represent facets of a
             neurobiological endophenotype linked to socioeconomic
             conditions of early development.},
   Language = {eng},
   Doi = {10.1093/cercor/bhq160},
   Key = {Gianaros2011}
}

@article{fds252004,
   Author = {Hariri, AR and Whalen, PJ},
   Title = {Face to face with the emotional brain},
   Journal = {Scientist (Philadelphia, Pa.)},
   Volume = {25},
   Number = {2},
   Pages = {30-},
   Year = {2011},
   ISSN = {0890-3670},
   Key = {fds252004}
}

@article{Nikolova2011,
   Author = {Nikolova, YS and Ferrell, RE and Manuck, SB and Hariri,
             AR},
   Title = {Multilocus genetic profile for dopamine signaling predicts
             ventral striatum reactivity},
   Journal = {Neuropsychopharmacology (Nature)},
   Volume = {36},
   Number = {9},
   Pages = {1940-1947},
   Address = {Department of Psychology and Neuroscience, Duke University,
             Durham, NC, USA.},
   Year = {2011},
   ISSN = {0893-133X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/21593733},
   Keywords = {Adult • Basal Ganglia/*metabolism/physiopathology
             • Cohort Studies • Dopamine/genetics/*physiology
             • Dopamine Plasma Membrane Transport Proteins/genetics
             • Female • Gene Expression Profiling/*methods
             • Genetic Loci/*genetics • Genetic Predisposition
             to Disease/genetics • Humans • Male • Middle
             Aged • Mood Disorders/diagnosis/*genetics/physiopathology
             • Polymorphism, Genetic/genetics • Predictive
             Value of Tests • Receptors, Dopamine D2/genetics •
             Receptors, Dopamine D4/genetics • Signal
             Transduction/*genetics},
   Abstract = {Research integrating neuroimaging and molecular genetics has
             yielded important insights into how variability in brain
             chemistry predicts individual differences in brain function,
             behavior and related risk for psychopathology. However,
             existing studies have been limited by their focus on the
             independent effects of single polymorphisms with modest
             impact on brain chemistry. Here, we explored the effects of
             five functional polymorphisms affecting dopamine (DA)
             signaling on reward-related ventral striatum (VS)
             reactivity, measured with BOLD fMRI, in a sample of 69
             Caucasians. We also compiled individual multilocus genetic
             profile scores reflecting the additive effects of alleles
             conferring relatively increased DA signaling across the five
             polymorphic loci: DAT1 9-repeat, DRD4 7-repeat, DRD2-141C
             Del, DRD2 Taq1A C (A2), and COMT 158 Met. These multilocus
             DA profile scores accounted for 10.9% of the
             inter-individual variability in reward-related VS
             reactivity. In contrast, none of the individual
             polymorphisms accounted for significant variability. Our
             results show that biologically informed multilocus genetic
             profiles have unique promise as indices of variability in
             brain chemistry that may yield advances in mapping
             individual differences in behaviorally relevant brain
             function. In turn, such genetic profiles may fuel
             gene-environment interactions research establishing
             trajectories of risk for psychopathology. © 2011 American
             College of Neuropsychopharmacology. All rights
             reserved.},
   Language = {eng},
   Doi = {10.1038/npp.2011.82},
   Key = {Nikolova2011}
}

@article{Carre2011,
   Author = {Carré, JM and McCormick, CM and Hariri, AR},
   Title = {The social neuroendocrinology of human aggression},
   Journal = {Psychoneuroendocrinology},
   Volume = {36},
   Number = {7},
   Pages = {935-944},
   Address = {Department of Psychology and Neuroscience, Duke University,
             Durham, NC, USA. justin.carre@duke.edu},
   Year = {2011},
   ISSN = {0306-4530},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/21367531},
   Keywords = {Aggression/*physiology/psychology • Animals •
             Competitive Behavior/physiology • Humans • Models,
             Animal • Models, Biological • Neural
             Pathways/metabolism/physiology • Neuroendocrinology
             • Neurosecretory Systems/metabolism/*physiology •
             *Social Behavior • Testosterone/blood/physiology},
   Abstract = {Testosterone concentrations fluctuate rapidly in response to
             competitive and aggressive interactions, suggesting that
             changes in testosterone rather than baseline differences
             shape ongoing and/or future competitive and aggressive
             behaviors. Although recent experiments in animal models
             provide compelling empirical support for this idea, studies
             in humans have focused largely on how competitive
             interactions drive changes in testosterone concentrations
             and not how these changes influence subsequent behavior. In
             this paper, we provide a review of the literature on
             testosterone and human aggression with a main focus on the
             role of testosterone dynamics in modulating reactive
             aggression. We also speculate on one putative neural
             mechanism through which testosterone may bias human
             aggressive behavior. Finally, we conclude by highlighting
             important questions that should be addressed in future
             research. © 2011 Elsevier Ltd.},
   Language = {eng},
   Doi = {10.1016/j.psyneuen.2011.02.001},
   Key = {Carre2011}
}

@article{Beevers2011,
   Author = {Beevers, CG and Marti, CN and Lee, H-J and Stote, DL and Ferrell, RE and Hariri, AR and Telch, MJ},
   Title = {Associations between serotonin transporter gene promoter
             region (5-HTTLPR) polymorphism and gaze bias for emotional
             information},
   Journal = {Journal of Abnormal Psychology},
   Volume = {120},
   Number = {1},
   Pages = {187-197},
   Address = {Department of Psychology, University of Texas at Austin, 1
             University Station, A8000, Austin, TX 78712, USA.
             beevers@psy.utexas.edu},
   Year = {2011},
   ISSN = {0021-843X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/21319930},
   Keywords = {Adult • Alleles • Analysis of Variance •
             Attention/*physiology • Emotions/*physiology • Eye
             Movements/*genetics • Facial Expression • Female
             • Gene Frequency • Genotype • Humans •
             Male • Photic Stimulation • *Polymorphism, Single
             Nucleotide • Promoter Regions, Genetic • Serotonin
             Plasma Membrane Transport Proteins/*genetics • Time
             Factors},
   Abstract = {The serotonin transporter promoter region polymorphism
             (5-HTTLPR) is associated with neural response to negative
             images in brain regions involved in the experience of
             emotion. However, the behavioral implications of this
             sensitivity have been studied far less extensively. The
             current study used eye-tracking methodology to examine how
             individuals genotyped for the 5-HTTLPR, including the single
             nucleotide polymorphism (SNP) rs25531, allocated attention
             during prolonged (30-s) exposure to face stimuli depicting
             positive and negative emotion. Short 5-HTTLPR allele
             carriers and carriers of the long allele with guanine at the
             sixth nucleotide (S/LG) displayed a stronger gaze bias
             (total fixation time, number of fixations, mean fixation
             length) for positive than for sad, threat, or neutral
             stimuli. In contrast, those homozygous for the long 5-HTTLPR
             allele with adenine at the sixth nucleotide (LA) viewed the
             emotion stimuli in an unbiased fashion. Time course analyses
             indicated no initial 5-HTTLPR group differences; however,
             S/LG 5-HTTLPR allele carriers were more likely than LA
             5-HTTLPR homozygotes to direct gaze toward happy than toward
             sad stimuli over time. This bias toward positive stimuli
             during the later stages of information processing likely
             reflects a strategic effort to downregulate heightened
             reactivity to negative stimuli among 5-HTTLPR S/LG allele
             carriers. © 2011 American Psychological
             Association.},
   Language = {eng},
   Doi = {10.1037/a0022125},
   Key = {Beevers2011}
}

@article{Hariri2011c,
   Author = {Hariri, AR},
   Title = {The what, where, and when of catechol-O-methyltransferase},
   Journal = {Biological Psychiatry},
   Volume = {70},
   Number = {3},
   Pages = {214-215},
   Address = {Laboratory of NeuroGenetics, Department of Psychology and
             Neuroscience, Institute for Genome Sciences and Policy, Duke
             University, 417 Chapel Drive, Durham, NC 27708, USA.
             ahmad.hariri@duke.edu},
   Year = {2011},
   ISSN = {0006-3223},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/21745617},
   Keywords = {Attention Deficit Disorder with Hyperactivity/*genetics
             • Brain/*physiology • Catechol
             O-Methyltransferase/*genetics • Central Nervous System
             Stimulants/*therapeutic use • Female • Humans
             • Male • Memory, Short-Term/*physiology •
             Methylphenidate/*therapeutic use • *Polymorphism,
             Single Nucleotide},
   Language = {eng},
   Doi = {10.1016/j.biopsych.2011.06.002},
   Key = {Hariri2011c}
}

@article{Hariri2011b,
   Author = {Hariri, AR and Shin, LM},
   Title = {Welcome to biology of mood \& anxiety disorders},
   Journal = {Biology of mood \& anxiety disorders},
   Volume = {1},
   Number = {1},
   Pages = {1},
   Address = {Laboratory of NeuroGenetics, Department of Psychology \&
             Neuroscience, Institute for Genome Sciences \& Policy, Duke
             University, Durham, NC USA. ahmad.hariri@duke.edu.},
   Year = {2011},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/22738418},
   Language = {eng},
   Doi = {10.1186/2045-5380-1-1},
   Key = {Hariri2011b}
}

@article{Hariri2011a,
   Author = {Hariri, AR and Whalen, PJ},
   Title = {The amygdala: Inside and out},
   Journal = {F1000 Biology Reports},
   Volume = {3},
   Number = {1},
   Pages = {2},
   Year = {2011},
   ISSN = {1740-4118},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/21399763},
   Abstract = {Research at the interface of psychology, neuroscience,
             molecular biology, and genetics, focusing on the amygdala,
             has begun to reveal a rule book for emotional reactions.
             Variations in intrinsic and extrinsic factors tweak the
             sensitivity of the amygdala, giving rise to differences in
             behavior between individuals. At their most extreme, these
             variations may generate psychological disorders, and even
             our current rudimentary understanding of this brain region
             suggests novel strategies for the treatment of such
             disorders. © 2011 Faculty of 1000 Ltd.},
   Language = {eng},
   Doi = {10.3410/B3-2},
   Key = {Hariri2011a}
}

@article{Hyde2011b,
   Author = {Hyde, LW and Bogdan, R and Hariri, AR},
   Title = {Understanding risk for psychopathology through imaging
             gene-environment interactions},
   Journal = {Trends in Cognitive Sciences},
   Volume = {15},
   Number = {9},
   Pages = {417-427},
   Address = {Department of Psychology and Center for the Neural Basis of
             Cognition, University of Pittsburgh, 210 South Bouquet St,
             Pittsburgh, PA 15260, USA. LWH2@pitt.edu},
   Year = {2011},
   ISSN = {1364-6613},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/21839667},
   Keywords = {Brain/*pathology/physiopathology • Epigenomics •
             *Gene-Environment Interaction • *Genetic Predisposition
             to Disease • Humans • Models, Biological •
             Neuroimaging • *Psychopathology},
   Abstract = {Examining the interplay of genes, experience and the brain
             is crucial to understanding psychopathology. We review the
             recent gene-environment interaction (G × E) and imaging
             genetics literature with the goal of developing models to
             bridge these approaches within single imaging
             gene-environment interaction (IG. × E) studies. We explore
             challenges inherent in both G × E and imaging genetics and
             highlight studies that address these limitations. In
             specifying IG × E models, we examine statistical methods
             for combining these approaches, and explore plausible
             biological mechanisms (e.g. epigenetics) through which these
             conditional mechanisms can be understood. Finally, we
             discuss the potential contribution that IG × E studies can
             make to understanding psychopathology and developing more
             personalized and effective prevention and treatment. © 2011
             Elsevier Ltd.},
   Language = {eng},
   Doi = {10.1016/j.tics.2011.07.001},
   Key = {Hyde2011b}
}

@article{Drabant2011,
   Author = {Drabant, EM and Kuo, JR and Ramel, W and Blechert, J and Edge, MD and Cooper, JR and Goldin, PR and Hariri, AR and Gross,
             JJ},
   Title = {Experiential, autonomic, and neural responses during threat
             anticipation vary as a function of threat intensity and
             neuroticism},
   Journal = {NeuroImage},
   Volume = {55},
   Number = {1},
   Pages = {401-410},
   Address = {Psychology Department, Stanford University, Stanford, CA
             94305, USA. drabant@stanford.edu},
   Year = {2011},
   ISSN = {1053-8119},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/21093595},
   Keywords = {Brain/*physiopathology • *Fear • Female •
             Humans • *Magnetic Resonance Imaging • Neurotic
             Disorders/*physiopathology • *Personal Autonomy •
             *Problem-Based Learning • Young Adult},
   Abstract = {Anticipatory emotional responses play a crucial role in
             preparing individuals for impending challenges. They do this
             by triggering a coordinated set of changes in behavioral,
             autonomic, and neural response systems. In the present
             study, we examined the biobehavioral impact of varying
             levels of anticipatory anxiety, using a shock anticipation
             task in which unpredictable electric shocks were threatened
             and delivered to the wrist at variable intervals and
             intensities (safe, medium, strong). This permitted
             investigation of a dynamic range of anticipatory anxiety
             responses. In two studies, 95 and 51 healthy female
             participants, respectively, underwent this shock
             anticipation task while providing continuous ratings of
             anxiety experience and electrodermal responding (Study 1)
             and during fMRI BOLD neuroimaging (Study 2). Results
             indicated a step-wise pattern of responding in anxiety
             experience and electrodermal responses. Several brain
             regions showed robust responses to shock anticipation
             relative to safe trials, including the hypothalamus,
             periaqueductal gray, caudate, precentral gyrus, thalamus,
             insula, ventrolateral PFC, dorsomedial PFC, and ACC. A
             subset of these regions demonstrated a linear pattern of
             increased responding from safe to medium to strong trials,
             including the bilateral insula, ACC, and inferior frontal
             gyrus. These responses were modulated by individual
             differences in neuroticism, such that those high in
             neuroticism showed exaggerated anxiety experience across the
             entire task, and reduced brain activation from medium to
             strong trials in a subset of brain regions. These findings
             suggest that individual differences in neuroticism may
             influence sensitivity to anticipatory threat and provide new
             insights into the mechanism through which neuroticism may
             confer risk for developing anxiety disorders via
             dysregulated anticipatory responses. © 2010 Elsevier
             Inc.},
   Language = {eng},
   Doi = {10.1016/j.neuroimage.2010.11.040},
   Key = {Drabant2011}
}

@article{Hyde2011a,
   Author = {Hyde, LW and Gorka, A and Manuck, SB and Hariri, AR},
   Title = {Perceived social support moderates the link between
             threat-related amygdala reactivity and trait
             anxiety},
   Journal = {Neuropsychologia},
   Volume = {49},
   Number = {4},
   Pages = {651-656},
   Address = {Department of Psychology, University of Pittsburgh,
             Pittsburgh, PA 15260, USA. lwh2@pitt.edu},
   Year = {2011},
   ISSN = {0028-3932},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/20813118},
   Keywords = {*Adaptation, Psychological • Adult •
             Aggression/*psychology • Amygdala/*physiology •
             Anxiety/*psychology • Brain Mapping • Female
             • Humans • Magnetic Resonance Imaging • Male
             • Middle Aged • Reference Values • *Social
             Support • Temperament},
   Abstract = {Several lines of research have illustrated that negative
             environments can precipitate psychopathology, particularly
             in the context of relatively increased biological risk,
             while social resources can buffer the effects of these
             environments. However, little research has examined how
             social resources might buffer proximal biological risk for
             psychopathology or the neurobiological pathways through
             which such buffering may be mediated. Here we report that
             the expression of trait anxiety as a function of
             threat-related amygdala reactivity is moderated by perceived
             social support, a resource for coping with adversity. A
             significant positive correlation between amygdala reactivity
             and trait anxiety was evident in individuals reporting below
             average levels of support but not in those reporting average
             or above average levels. These results were consistent
             across multiple measures of trait anxiety and were specific
             to anxiety in that they did not extend to measures of broad
             negative or positive affect. Our findings illuminate a
             biological pathway, namely moderation of amygdala-related
             anxiety, through which social support may confer resilience
             to psychopathology. Moreover, our results indicate that
             links between neural reactivity and behavior are not static
             but rather may be contingent on social resources. © 2010
             Elsevier Ltd.},
   Language = {eng},
   Doi = {10.1016/j.neuropsychologia.2010.08.025},
   Key = {Hyde2011a}
}

@article{fds252110,
   Author = {Carre, JM and Murphy, KR and Hariri, AR},
   Title = {What lies beneath the face of aggression?},
   Journal = {Social cognitive and affective neuroscience},
   Year = {2011},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/22198969},
   Abstract = {Recent evidence indicates that a sexually dimorphic feature
             of humans, the facial width-to-height ratio (FWHR), is
             positively correlated with reactive aggression, particularly
             in men. Also, predictions about the aggressive tendencies of
             others faithfully map onto FWHR in the absence of explicit
             awareness of this metric. Here, we provide the first
             evidence that amygdala reactivity to social signals of
             interpersonal challenge may underlie the link between
             aggression and the FWHR. Specifically, amygdala reactivity
             to angry faces was positively correlated with aggression,
             but only among men with relatively large FWHRs. The patterns
             of association were specific to angry facial expressions and
             unique to men. These links may reflect the common influence
             of pubertal testosterone on craniofacial growth and
             development of neural circuitry underlying aggression.
             Amygdala reactivity may also represent a plausible pathway
             through which FWHR may have evolved to represent an honest
             indicator of conspecific threat, namely by reflecting the
             responsiveness of neural circuitry mediating aggressive
             behavior.},
   Doi = {10.1093/scan/nsr096},
   Key = {fds252110}
}

@article{Fisher2011,
   Author = {Fisher, PM and Price, JC and Meltzer, CC and Moses Kolko and EL and Becker,
             C and Berga, SL and Hariri, AR},
   Title = {Medial prefrontal cortex serotonin 1A and 2A receptor
             binding interacts to predict threat-related amygdala
             reactivity},
   Journal = {Biology of mood \& anxiety disorders},
   Volume = {1},
   Number = {1},
   Pages = {2},
   Address = {Center for Neuroscience, University of Pittsburgh,
             Pittsburgh, Pennsylvania 15260, USA. patrick.fisher@gmail.com.},
   Year = {2011},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/22738071},
   Abstract = {BACKGROUND: The amygdala and medial prefrontal cortex (mPFC)
             comprise a key corticolimbic circuit that helps shape
             individual differences in sensitivity to threat and the
             related risk for psychopathology. Although serotonin (5-HT)
             is known to be a key modulator of this circuit, the specific
             receptors mediating this modulation are unclear. The
             colocalization of 5-HT1A and 5-HT2A receptors on mPFC
             glutamatergic neurons suggests that their functional
             interactions may mediate 5-HT effects on this circuit
             through top-down regulation of amygdala reactivity. Using a
             multimodal neuroimaging strategy in 39 healthy volunteers,
             we determined whether threat-related amygdala reactivity,
             assessed with blood oxygen level-dependent functional
             magnetic resonance imaging, was significantly predicted by
             the interaction between mPFC 5-HT1A and 5-HT2A receptor
             levels, assessed by positron emission tomography. RESULTS:
             5-HT1A binding in the mPFC significantly moderated an
             inverse correlation between mPFC 5-HT2A binding and
             threat-related amygdala reactivity. Specifically, mPFC
             5-HT2A binding was significantly inversely correlated with
             amygdala reactivity only when mPFC 5-HT1A binding was
             relatively low. CONCLUSIONS: Our findings provide evidence
             that 5-HT1A and 5-HT2A receptors interact to shape
             serotonergic modulation of a functional circuit between the
             amygdala and mPFC. The effect of the interaction between
             mPFC 5-HT1A and 5-HT2A binding and amygdala reactivity is
             consistent with the colocalization of these receptors on
             glutamatergic neurons in the mPFC.},
   Language = {eng},
   Doi = {10.1186/2045-5380-1-2},
   Key = {Fisher2011}
}

@article{fds251971,
   Author = {Hariri, AR and Weinberger, DR},
   Title = {Genetics of Human Anxiety and Its Disorders},
   Pages = {669-677},
   Year = {2010},
   Month = {December},
   url = {http://dx.doi.org/10.1016/B978-008045046-9.00845-7},
   Abstract = {Normal variation in human emotionality, in temperament and
             risk for affective disorders, is explained to a large degree
             by genetic variation. The sequencing of the human genome has
             made it possible to test the role of specific genes on
             measures of human emotionality, on risk for affective
             disorders, and on the brain systems that appear to mediate
             emotion-related phenotypes. A novel approach, called imaging
             genetics, has shown that several genes that impact on brain
             serotonergic signaling affect the development and function
             of circuits of the limbic system involved in emotional
             experience and behavior. © 2009 Published by
             null.},
   Doi = {10.1016/B978-008045046-9.00845-7},
   Key = {fds251971}
}

@article{Caspi2010,
   Author = {Caspi, A and Hariri, AR and Holmes, A and Uher, R and Moffitt,
             TE},
   Title = {Genetic sensitivity to the environment: the case of the
             serotonin transporter gene and its implications for studying
             complex diseases and traits.},
   Journal = {American Journal of Psychiatry},
   Volume = {167},
   Number = {5},
   Pages = {509-527},
   Address = {Department of Psychology, and Institute for Genome Sciences
             and Policy, Duke University, Durham, NC 27708, USA.
             ac115@duke.edu},
   Year = {2010},
   Month = {May},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/20231323},
   Keywords = {Animals • Brain/pathology/physiopathology •
             Depressive Disorder/genetics • Environment •
             Genetic Predisposition to Disease/*genetics •
             Genome-Wide Association Study/methods • Genotype •
             Humans • Models, Psychological • Mood
             Disorders/genetics • Primates/genetics/psychology
             • Serotonin Plasma Membrane Transport
             Proteins/*genetics/physiology • Stress,
             Psychological/complications/*genetics},
   Abstract = {Evidence of marked variability in response among people
             exposed to the same environmental risk implies that
             individual differences in genetic susceptibility might be at
             work. The study of such Gene-by-Environment (GxE)
             interactions has gained momentum. In this article, the
             authors review research about one of the most extensive
             areas of inquiry: variation in the promoter region of the
             serotonin transporter gene (SLC6A4; also known as 5-HTT) and
             its contribution to stress sensitivity. Research in this
             area has both advanced basic science and generated broader
             lessons for studying complex diseases and traits. The
             authors evaluate four lines of evidence about the 5-HTT
             stress-sensitivity hypothesis: 1) observational studies
             about the serotonin transporter linked polymorphic region
             (5-HTTLPR), stress sensitivity, and depression in humans; 2)
             experimental neuroscience studies about the 5-HTTLPR and
             biological phenotypes relevant to the human stress response;
             3) studies of 5-HTT variation and stress sensitivity in
             nonhuman primates; and 4) studies of stress sensitivity and
             genetically engineered 5-HTT mutations in rodents. The
             authors then dispel some misconceptions and offer
             recommendations for GxE research. The authors discuss how
             GxE interaction hypotheses can be tested with large and
             small samples, how GxE research can be carried out before as
             well as after replicated gene discovery, the uses of GxE
             research as a tool for gene discovery, the importance of
             construct validation in evaluating GxE research, and the
             contribution of GxE research to the public understanding of
             genetic science.},
   Language = {eng},
   Doi = {10.1176/appi.ajp.2010.09101452},
   Key = {Caspi2010}
}

@article{fds252003,
   Author = {Jedema, HP and Gianaros, PJ and Greer, PJ and Kerr, DD and Liu, S and Higley, JD and Suomi, SJ and Olsen, AS and Porter, JN and Lopresti, BJ and Hariri, AR and Bradberry, CW},
   Title = {Morphological differences associated with a serotonin
             transporter polymorphism (5-HTTLPR) in rhesus
             macaques},
   Journal = {Molecular Psychiatry},
   Volume = {15},
   Number = {5},
   Pages = {446-},
   Year = {2010},
   ISSN = {1359-4184},
   url = {http://dx.doi.org/10.1038/mp.2010.49},
   Doi = {10.1038/mp.2010.49},
   Key = {fds252003}
}

@article{Manuck2010,
   Author = {Manuck, SB and Marsland, AL and Flory, JD and Gorka, A and Ferrell, RE and Hariri, AR},
   Title = {Salivary testosterone and a trinucleotide (CAG) length
             polymorphism in the androgen receptor gene predict amygdala
             reactivity in men},
   Journal = {Psychoneuroendocrinology},
   Volume = {35},
   Number = {1},
   Pages = {94-104},
   Address = {Department of Psychology, University of Pittsburgh,
             Pittsburgh, PA 15260, United States. Manuck@pitt.edu},
   Year = {2010},
   ISSN = {0306-4530},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/19493626},
   Keywords = {Adult • Amygdala/*physiology • DNA/genetics •
             Facial Expression • Genotype • Humans • Image
             Processing, Computer-Assisted • Individuality •
             Magnetic Resonance Imaging • Male • Middle Aged
             • Oxygen/blood • Polymorphism, Genetic •
             Receptors, Androgen/*genetics/physiology •
             Saliva/*metabolism • Social Perception •
             Testosterone/*metabolism • Trinucleotide
             Repeats/*genetics},
   Abstract = {In studies employing functional magnetic resonance imaging
             (fMRI), reactivity of the amygdala to threat-related sensory
             cues (viz., facial displays of negative emotion) has been
             found to correlate positively with interindividual
             variability in testosterone levels of women and young men
             and to increase on acute administration of exogenous
             testosterone. Many of the biological actions of testosterone
             are mediated by intracellular androgen receptors (ARs),
             which exert transcriptional control of androgen-dependent
             genes and are expressed in various regions of the brain,
             including the amygdala. Transactivation potential of the AR
             decreases (yielding relative androgen insensitivity) with
             expansion a polyglutamine stretch in the N-terminal domain
             of the AR protein, as encoded by a trinucleotide (CAG)
             repeat polymorphism in exon 1 of the X-chromosome AR gene.
             Here we examined whether amygdala reactivity to
             threat-related facial expressions (fear, anger) differs as a
             function of AR CAG length variation and endogenous
             (salivary) testosterone in a mid-life sample of 41 healthy
             men (mean age = 45.6 years, range: 34-54 years; CAG repeats,
             range: 19-29). Testosterone correlated inversely with
             participant age (r = -0.39, p = 0.012) and positively with
             number of CAG repeats (r = 0.45, p = 0.003). In partial
             correlations adjusted for testosterone level, reactivity in
             the ventral amygdala was lowest among men with largest
             number of CAG repeats. This inverse association was seen in
             both the right (rp = -0.34, p &lt; 0.05) and left (rp =
             -0.32, p &lt; 0.05) hemisphere. Activation of dorsal
             amygdala, correlated positively with individual differences
             in salivary testosterone, also in right (r = 0.40, p &lt;
             0.02) and left (r = 0.32, p &lt; 0.05) hemisphere, but was
             not affected by number of CAG repeats. Hence, androgenic
             influences on threat-related reactivity in the ventral
             amygdala may be moderated partially by CAG length variation
             in the AR gene. Because individual differences in salivary
             testosterone also predicted dorsal amygdala reactivity and
             did so independently of CAG repeats, it is suggested that
             androgenic influences within this anatomically distinct
             region may be mediated, in part, by non-genomic or
             AR-independent mechanisms. © 2009 Elsevier Ltd. All rights
             reserved.},
   Language = {eng},
   Doi = {10.1016/j.psyneuen.2009.04.013},
   Key = {Manuck2010}
}

@article{Munoz2010,
   Author = {Muñoz, KE and Meyer-Lindenberg, A and Hariri, AR and Mervis, CB and Mattay, VS and Morris, CA and Berman, KF},
   Title = {Abnormalities in neural processing of emotional stimuli in
             Williams syndrome vary according to social vs. non-social
             content},
   Journal = {NeuroImage},
   Volume = {50},
   Number = {1},
   Pages = {340-346},
   Address = {Section on Integrative Neuroimaging, National Institute of
             Mental Health, NIH, DHHS, Bethesda, MD 20892,
             USA.},
   Year = {2010},
   ISSN = {1053-8119},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/20004252},
   Keywords = {Adult • Amygdala/physiopathology •
             Brain/*physiopathology • Brain Mapping •
             Cognition/*physiology • Emotions/*physiology •
             Female • Humans • Intelligence • Intelligence
             Tests • Magnetic Resonance Imaging • Male •
             Neural Pathways/physiopathology • Oxygen/blood •
             Prefrontal Cortex/physiopathology • *Social Behavior
             • Visual Perception/physiology • Williams
             Syndrome/*physiopathology},
   Abstract = {Williams syndrome (WS) is a rare genetic disorder caused by
             the deletion of ∼ 25 genes on chromosome 7q11.23 and is
             characterized by both hypersociability and increases in
             specific phobia and anticipatory anxiety regarding
             non-social entities or circumstances. Alterations in
             amygdala reactivity and prefrontal regulation consistent
             with the observed behavioral pattern of social versus
             non-social abnormalities have been previously demonstrated
             in individuals with WS (Meyer-Lindenberg et al., 2005).
             However, in that study, the social stimulus (faces) matching
             task was more difficult than the non-social scene (IAPS
             stimuli) matching task, making it impossible to disambiguate
             the relative contributions of task difficulty and stimulus
             type (social versus non-social). In the present study, we
             examined the performance of the same group of participants
             with WS and normal IQs during a more cognitively demanding
             task using the same scene stimuli as in the prior study.
             Confirming previous findings, the results indicated (a) a
             differential response of prefrontal regions as a function of
             task difficulty and (b) a persistently increased activation
             of the amygdala to non-social scenes by individuals with WS
             regardless of cognitive load. These data provide further
             evidence of disruption in amygdala-prefrontal circuitry in
             individuals with WS. © 2009.},
   Language = {eng},
   Doi = {10.1016/j.neuroimage.2009.11.069},
   Key = {Munoz2010}
}

@article{Hariri2010,
   Author = {Hariri, AR},
   Title = {Genetic polymorphisms: A cornerstone of translational
             biobehavioral research},
   Journal = {Science Translational Medicine},
   Volume = {2},
   Number = {18},
   Pages = {18ps6},
   Address = {Department of Psychology and Neuroscience, Institute for
             Genome Sciences and Policy, Duke University, Durham, NC
             27708, USA. ahmad.hariri@duke.edu},
   Year = {2010},
   ISSN = {1946-6234},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/20371481},
   Keywords = {Amino Acid Substitution/genetics • Animals •
             *Behavior • Brain-Derived Neurotrophic Factor/genetics
             • Humans • Mice • *Polymorphism, Genetic
             • *Translational Medical Research},
   Abstract = {A new generation of interdisciplinary research seeks to use
             common functional genetic polymorphisms to model emergent
             variability in brain chemistry that regulates behaviorally
             relevant brain structure and function. This genetically
             mediated variability is then being mapped onto trajectories
             of risk for psychopathology, especially that precipitated by
             environmental adversity. This Perspective highlights a
             recent paper in Science that provides a powerful example of
             how a common functional genetic polymorphism can serve as a
             translational bridge between human and mouse research,
             extending our understanding of biological pathways that
             mediate individual differences in behavior and in risk for
             psychopathology.},
   Language = {eng},
   Doi = {10.1126/scitranslmed.3000811},
   Key = {Hariri2010}
}

@article{Salgado-Pineda2010,
   Author = {Salgado-Pineda, P and Fakra, E and Delaveau, P and Hariri, AR and Blin,
             O},
   Title = {Differential patterns of initial and sustained responses in
             amygdala and cortical regions to emotional stimuli in
             schizophrenia patients and healthy participants},
   Journal = {Journal of psychiatry & neuroscience : JPN},
   Volume = {35},
   Number = {1},
   Pages = {41-48},
   Address = {Centre d'Investigation Clinique-Unite de Pharmacologie
             Clinique et d'Evaluations Therapeutiques, Hopital de la
             Timone, Unite Mixte de Recherche, Centre national de la
             recherche scientifique, 6193 Institut de Neurosciences
             Cognitives de la Mediterranee, Ma},
   Year = {2010},
   ISSN = {1180-4882},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/20040245},
   Keywords = {Adult • Amygdala/*physiopathology • Brain Mapping
             • Cerebral Cortex/*physiopathology •
             Emotions/*physiology • Executive Function/*physiology
             • Facial Expression • Female • Humans •
             Magnetic Resonance Imaging • Male • Middle Aged
             • Neural Pathways/physiopathology •
             Neuropsychological Tests • Pattern Recognition,
             Visual/physiology • Psychiatric Status Rating Scales
             • Reaction Time • Schizophrenia/*physiopathology
             • Time Factors • Young Adult},
   Abstract = {Background: We sought to investigate the altered brain
             responses to emotional stimuli in patients with
             schizophrenia. Methods: We analyzed data from 14 patients
             with schizophrenia and 14 healthy controls who performed an
             emotional face matching task. We evaluated brain activity
             and connectivity in the amygdala and cortical regions during
             the initial (first 21 seconds of each stimulation block) and
             sustained (last 21 seconds) stages of an emotional
             processing task, and we determined changes in amygdala
             activity across the emotional processing task. Results: The
             patients with schizophrenia showed similar amygdala
             activation to the controls during the initial stage of
             processing, but their activation decreased during the
             sustained stage. The controls showed increasing amygdala
             activity across the emotional blocks, whereas activity
             progressively decreased in the schizophrenia group. The
             patients with schizophrenia showed increased cortical
             activity and interconnectivity in the medial frontal and
             inferior parietal cortex in the initial stage of emotional
             processing. There was increased activity in the superior
             temporal cortex and greater connectivity with the inferior
             parietal cortex in the sustained stage. Performance accuracy
             was lower in the schizophrenia group in the first part of
             the block, while their reaction time was longer in the
             latter part of the block. Limitations: It was not possible
             to specify the moment at which the switch in amygdala
             response occurred. Conclusion: Our findings suggest that
             patients with schizophrenia have an initial automatic
             emotional response but that they need to switch to a
             compensatory cognitive strategy to solve the task. © 2010
             Canadian Medical Association.},
   Language = {eng},
   Doi = {10.1503/jpn.090017},
   Key = {Salgado-Pineda2010}
}

@article{Jedema2010,
   Author = {Jedema, HP and Gianaros, PJ and Greer, PJ and Kerr, DD and Liu, S and Higley, JD and Suomi, SJ and Olsen, AS and Porter, JN and Lopresti, BJ and Hariri, AR and Bradberry, CW},
   Title = {Cognitive impact of genetic variation of the serotonin
             transporter in primates is associated with differences in
             brain morphology rather than serotonin neurotransmission},
   Journal = {Molecular Psychiatry},
   Volume = {15},
   Number = {5},
   Pages = {512-522},
   Address = {Department of Psychiatry, University of Pittsburgh,
             Pittsburgh, PA 15261, USA.},
   Year = {2010},
   ISSN = {1359-4184},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/19721434},
   Keywords = {Animals • Avoidance Learning/physiology •
             Behavior, Animal/physiology • Benzylamines/metabolism
             • Brain/drug effects/radionuclide imaging • Brain
             Mapping • Carbon Isotopes/metabolism • Choice
             Behavior/*physiology • Cognition/*physiology •
             Genotype • Macaca mulatta • Magnetic Resonance
             Imaging/methods • Male • Neuropsychological Tests
             • Piperazines/metabolism • Polymorphism,
             Genetic/*genetics • Positron-Emission
             Tomography/methods • Protein Binding/drug
             effects/genetics • Pyridines/metabolism •
             Receptor, Serotonin, 5-HT1A/genetics •
             Serotonin/genetics/*metabolism • Serotonin Plasma
             Membrane Transport Proteins/*genetics • Synaptic
             Transmission/*genetics • Time Factors •
             Tritium/metabolism},
   Abstract = {A powerful convergence of genetics, neuroimaging and
             epidemiological research has identified the biological
             pathways mediating individual differences in complex
             behavioral processes and the related risk for disease.
             Orthologous genetic variation in non-human primates (NHPs)
             represents a unique opportunity to characterize the detailed
             molecular and cellular mechanisms that bias behaviorally and
             clinically relevant brain function. We report that a rhesus
             macaque orthologue of a common polymorphism of the serotonin
             transporter gene (rh5-HTTLPR) has strikingly similar effects
             on behavior and brain morphology to those in humans.
             Specifically, the rh5-HTTLPR (S)hort allele broadly affects
             cognitive choice behavior and brain morphology without
             observably affecting the 5-hydroxytryptamine (5-HT)
             transporter or 5-HT 1A concentrations in vivo. Collectively,
             our findings indicate that 5-HTTLPR-associated behavioral
             effects reflect genotype-dependent biases in cortical
             development rather than static differences in serotonergic
             signaling mechanisms. Moreover, these data highlight the
             vast potential of NHP models in advancing our understanding
             of human genetic variation affecting behavior and
             neuropsychiatric disease liability. © 2010 Nature
             Publishing Group All rights reserved.},
   Language = {eng},
   Doi = {10.1038/mp.2009.90},
   Key = {Jedema2010}
}

@article{Cornelius2010,
   Author = {Cornelius, JR and Aizenstein, HJ and Hariri, AR},
   Title = {Amygdala reactivity is inversely related to level of
             cannabis use in individuals with comorbid cannabis
             dependence and major depression},
   Journal = {Addictive Behaviors},
   Volume = {35},
   Number = {6},
   Pages = {644-646},
   Address = {Department of Psychiatry, University of Pittsburgh School of
             Medicine, Pittsburgh, PA 15213, United States.
             corneliusjr@upmc.edu},
   Year = {2010},
   ISSN = {0306-4603},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/20189314},
   Keywords = {Amygdala/*drug effects/physiopathology • Antidepressive
             Agents, Second-Generation/therapeutic use •
             Cannabis/*adverse effects • Comorbidity •
             Depressive Disorder/drug therapy/epidemiology •
             Diagnosis, Dual (Psychiatry) • Double-Blind Method
             • Fear/*drug effects • Female •
             Fluoxetine/therapeutic use • Humans • Magnetic
             Resonance Imaging/methods • Male • Marijuana
             Abuse/epidemiology/*physiopathology • Social Behavior
             • Young Adult},
   Abstract = {Phan et al. (2008) recently reported that an acute dose of
             oral THC is associated with a decrease in threat-related
             amygdala reactivity during a social threat stimulus task.
             However, to date, those findings have not been replicated,
             and have not been extended to clinical studies involving
             smoked rather than oral cannabis. In this study, we
             hypothesized that level of cannabis smoked by participants
             in our treatment study would be inversely related to the
             level of threat-related amygdala reactivity. Subjects were
             recruited from among participants in our double-blind,
             placebo-controlled trial of fluoxetine in comorbid youth
             with cannabis dependence/major depression. The
             threat-related amygdala reactivity task used by Hariri et
             al. (2009) was completed during BOLD fMRI scans at study
             baseline and then again 12 weeks later at the end of the
             trial. Data are available from six subjects with pre-and
             post-treatment fMRI data. During the course of the study,
             five of the six subjects demonstrated a decrease in their
             level of cannabis use, with a mean decrease of 64%, and
             those persons all demonstrated an increase in their level of
             amygdala reactivity. One subject demonstrated an increase in
             their level of cannabis use (a 79% increase) during the
             treatment trial, and that person demonstrated a decrease in
             their level of amygdala reactivity. Thus, a higher level of
             cannabis use was consistently associated with a lower level
             of amygdala reactivity across all subjects (matched pairs t
             = 2.70, df = 5, p &lt; 0.05, two-tailed). These findings are
             consistent with the reports by Phan et al. (2008) and Hariri
             et al. (2009) suggesting that cannabinoids have an
             inhibitory effect on threat-related amygdala reactivity. ©
             2010 Elsevier Ltd. All rights reserved.},
   Language = {eng},
   Doi = {10.1016/j.addbeh.2010.02.004},
   Key = {Cornelius2010}
}

@article{Chiao2010,
   Author = {Chiao, JY and Hariri, AR and Harada, T and Mano, Y and Sadato, N and Parrish, TB and Iidaka, T},
   Title = {Theory and methods in cultural neuroscience},
   Journal = {Social Cognitive and Affective Neuroscience},
   Volume = {5},
   Number = {2-3},
   Pages = {356-361},
   Address = {Department of Psychology and Interdepartmental Neuroscience
             Program, Northwestern University, Evanston, IL 60208, USA.
             jchiao@northwestern.edu},
   Year = {2010},
   ISSN = {1749-5016},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/20592044},
   Keywords = {Brain/physiology • Brain Mapping • Cross-Cultural
             Comparison • *Culture • Humans • Magnetic
             Resonance Imaging • Neurosciences/*methods •
             Polymorphism, Genetic/genetics • Research Design •
             Stereotyping},
   Abstract = {Cultural neuroscience is an emerging research discipline
             that investigates cultural variation in psychological,
             neural and genomic processes as a means of articulating the
             bidirectional relationship of these processes and their
             emergent properties. Research in cultural neuroscience
             integrates theory and methods from anthropology, cultural
             psychology, neuroscience and neurogenetics. Here, we review
             a set of core theoretical and methodological challenges
             facing researchers when planning and conducting cultural
             neuroscience studies, and provide suggestions for overcoming
             these challenges. In particular, we focus on the problems of
             defining culture and culturally appropriate experimental
             tasks, comparing neuroimaging data acquired from different
             populations and scanner sites and identifying functional
             genetic polymorphisms relevant to culture. Implications of
             cultural neuroscience research for addressing current issues
             in population health disparities are discussed. © The
             Author (2010). Published by Oxford University Press. For
             Permissions, please email: journals.permissions@oxfordjournals.org.},
   Language = {eng},
   Doi = {10.1093/scan/nsq063},
   Key = {Chiao2010}
}

@article{fds251972,
   Author = {Hariri, A},
   Title = {Imaging Genetics: Integration of Neuroimaging and Genetics
             in the Search for Predictive Markers},
   Journal = {Genomic and Personalized Medicine, Two-Vol
             Set},
   Pages = {532-537},
   Year = {2009},
   url = {http://dx.doi.org/10.1016/B978-0-12-369420-1.00047-0},
   Doi = {10.1016/B978-0-12-369420-1.00047-0},
   Key = {fds251972}
}

@article{fds252001,
   Author = {Zhou, Z and Zhu, G and Hariri, AR and Enoch, M-A and Scott, D and Sinha, R and Virkkunen, M and Mash, DC and Lipsky, RH and Hu, X-Z and Hodgkinson, CA and Xu, K and Buzas, B and Yuan, Q and Shen, P-H and Ferrell, RE and Manuck,
             SB and Brown, SM and Hauger, RL and Stohler, CS and Zubieta, J-K and Goldman, D},
   Title = {Zhou et al. reply},
   Journal = {Nature},
   Volume = {458},
   Number = {7238},
   Pages = {E7},
   Year = {2009},
   ISSN = {0028-0836},
   url = {http://dx.doi.org/10.1038/nature07928},
   Doi = {10.1038/nature07928},
   Key = {fds252001}
}

@article{fds252002,
   Author = {Hariri, AR},
   Title = {Ahmad R. Hariri: Award for Distinguished Scientific Early
             Career Contributions to Psychology},
   Journal = {American Psychologist},
   Volume = {64},
   Number = {8},
   Pages = {683-684},
   Year = {2009},
   ISSN = {0003-066X},
   url = {http://dx.doi.org/10.1037/a0016290},
   Doi = {10.1037/a0016290},
   Key = {fds252002}
}

@article{Mechelli2009,
   Author = {Mechelli, A and Tognin, S and McGuire, PK and Prata, D and Sartori, G and Fusar-Poli, P and Brito, SD and Hariri, AR and Viding,
             E},
   Title = {Genetic Vulnerability to Affective Psychopathology in
             Childhood: A Combined Voxel-Based Morphometry and Functional
             Magnetic Resonance Imaging Study},
   Journal = {Biological Psychiatry},
   Volume = {66},
   Number = {3},
   Pages = {231-237},
   Address = {Department of Psychology, Institute of Psychiatry, PO Box
             67, Division of Psychological Medicine and Psychiatry,
             King's College London, 103 Denmark Hill, London SE5 8AF,
             United Kingdom. a.mechelli@iop.kcl.ac.uk},
   Year = {2009},
   ISSN = {0006-3223},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/19278671},
   Keywords = {Affective Disorders, Psychotic/*genetics/*pathology •
             Brain/*blood supply/*pathology • Brain Mapping •
             Catechol O-Methyltransferase/*genetics • Child •
             Genotype • Humans • Image Processing,
             Computer-Assisted/methods • Longitudinal Studies •
             Magnetic Resonance Imaging/methods • Male •
             Methionine/genetics • Neuropsychological Tests •
             Oxygen/blood • Photic Stimulation • Polymorphism,
             Genetic/*drug effects • Reaction Time/physiology •
             Twin Studies as Topic • Valine/genetics},
   Abstract = {Background: The majority of affective psychopathology is
             rooted early in life and first emerges during childhood and
             adolescence. However, little is known about how genetic
             vulnerability affects brain structure and function in
             childhood since the vast majority of studies published so
             far have been conducted on adult participants. The present
             investigation examined for the first time the effects of
             catechol-O-methyltransferase (COMT) valine (val) 158
             methionine (met) (val158met) polymorphism, which has been
             shown to moderate predisposition to negative mood and
             affective disorders, on brain structure and function in
             children. Methods: Voxel-based morphometry and functional
             magnetic resonance imaging were used to measure gray matter
             volume and emotional reactivity in 50 children aged between
             10 and 12 years. We tested the hypothesis that met158 allele
             affects structural brain development and confers heightened
             reactivity within the affective frontolimbic circuit in
             children. Results: The met158 allele was positively
             associated with gray matter volume in the left hippocampal
             head where genotype accounted for 59% of interindividual
             variance. In addition, the met158 allele was positively
             associated with neuronal responses to fearful relative to
             neutral facial expressions in the right parahippocampal
             gyrus where genotype accounted for 14% of the
             interindividual variance. Conclusions: These results
             indicate that the met158 allele is associated with increased
             gray matter volume and heightened reactivity during
             emotional processing within the limbic system in children as
             young as 10 to 12 years of age. These findings are
             consistent with the notion that genetic factors affect brain
             function to moderate vulnerability to affective
             psychopathology from childhood. © 2009 Society of
             Biological Psychiatry.},
   Language = {eng},
   Doi = {10.1016/j.biopsych.2009.01.033},
   Key = {Mechelli2009}
}

@article{Blasi2009,
   Author = {Blasi, G and Hariri, AR and Alce, G and Taurisano, P and Sambataro, F and Das, S and Bertolino, A and Weinberger, DR and Mattay,
             VS},
   Title = {Preferential Amygdala Reactivity to the Negative Assessment
             of Neutral Faces},
   Journal = {Biological Psychiatry},
   Volume = {66},
   Number = {9},
   Pages = {847-853},
   Address = {Psychiatric Neuroscience Group, Department of Neurological
             and Psychiatric Sciences, University of Bari, Bari,
             Italy.},
   Year = {2009},
   ISSN = {0006-3223},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/19709644},
   Keywords = {Adult • Amygdala/*physiology • Brain Mapping
             • Decision Making/*physiology • Emotions •
             *Facial Expression • Female • Gyrus
             Cinguli/physiology • Humans • Magnetic Resonance
             Imaging • Male • Neural Pathways/physiology •
             Prefrontal Cortex/physiology • Prejudice •
             Reaction Time • Social Perception},
   Abstract = {Background: Prior studies suggest that the amygdala shapes
             complex behavioral responses to socially ambiguous cues. We
             explored human amygdala function during explicit behavioral
             decision making about discrete emotional facial expressions
             that can represent socially unambiguous and ambiguous cues.
             Methods: During functional magnetic resonance imaging, 43
             healthy adults were required to make complex social
             decisions (i.e., approach or avoid) about either relatively
             unambiguous (i.e., angry, fearful, happy) or ambiguous
             (i.e., neutral) facial expressions. Amygdala activation
             during this task was compared with that elicited by simple,
             perceptual decisions (sex discrimination) about the
             identical facial stimuli. Results: Angry and fearful
             expressions were more frequently judged as avoidable and
             happy expressions most often as approachable. Neutral
             expressions were equally judged as avoidable and
             approachable. Reaction times to neutral expressions were
             longer than those to angry, fearful, and happy expressions
             during social judgment only. Imaging data on stimuli judged
             to be avoided revealed a significant task by emotion
             interaction in the amygdala. Here, only neutral facial
             expressions elicited greater activity during social judgment
             than during sex discrimination. Furthermore, during social
             judgment only, neutral faces judged to be avoided were
             associated with greater amygdala activity relative to
             neutral faces that were judged as approachable. Moreover,
             functional coupling between the amygdala and both
             dorsolateral prefrontal (social judgment &gt; sex
             discrimination) and cingulate (sex discrimination &gt;
             social judgment) cortices was differentially modulated by
             task during processing of neutral faces. Conclusions: Our
             results suggest that increased amygdala reactivity and
             differential functional coupling with prefrontal circuitries
             may shape complex decisions and behavioral responses to
             socially ambiguous cues. © 2009 Society of Biological
             Psychiatry.},
   Language = {eng},
   Doi = {10.1016/j.biopsych.2009.06.017},
   Key = {Blasi2009}
}

@article{Forbes2009b,
   Author = {Forbes, EE and Brown, SM and Kimak, M and Ferrell, RE and Manuck, SB and Hariri, AR},
   Title = {Genetic variation in components of dopamine
             neurotransmission impacts ventral striatal reactivity
             associated with impulsivity},
   Journal = {Molecular Psychiatry},
   Volume = {14},
   Number = {1},
   Pages = {60-70},
   Address = {Department of Psychiatry, University of Pittsburgh,
             Pittsburgh, PA 15213, USA.},
   Year = {2009},
   ISSN = {1359-4184},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/17893706},
   Keywords = {Adult • Analysis of Variance • Basal Ganglia/blood
             supply/*physiopathology • Case-Control Studies •
             Catechol O-Methyltransferase/genetics •
             Dopamine/*genetics/metabolism • Dopamine Plasma
             Membrane Transport Proteins/genetics • Female •
             Gene Frequency • Genetic Variation/*genetics •
             Genotype • Humans • Image Processing,
             Computer-Assisted/methods • Impulsive
             Behavior/*genetics/*pathology • Magnetic Resonance
             Imaging/methods • Male • Middle Aged •
             Oxygen/blood • Receptors, Dopamine D3/genetics •
             Receptors, Dopamine D4/genetics • Reward •
             Synaptic Transmission/*genetics • Young
             Adult},
   Abstract = {Individual differences in traits such as impulsivity involve
             high reward sensitivity and are associated with risk for
             substance use disorders. The ventral striatum (VS) has been
             widely implicated in reward processing, and individual
             differences in its function are linked to these disorders.
             Dopamine (DA) plays a critical role in reward processing and
             is a potent neuromodulator of VS reactivity. Moreover,
             altered DA signaling has been associated with normal and
             pathological reward-related behaviors. Functional
             polymorphisms in DA-related genes represent an important
             source of variability in DA function that may subsequently
             impact VS reactivity and associated reward-related
             behaviors. Using an imaging genetics approach, we examined
             the modulatory effects of common, putatively functional
             DA-related polymorphisms on reward-related VS reactivity
             associated with self-reported impulsivity. Genetic variants
             associated with relatively increased striatal DA release
             (DRD2 -141C deletion) and availability (DAT1 9-repeat), as
             well as diminished inhibitory postsynaptic DA effects (DRD2
             -141C deletion and DRD4 7-repeat), predicted 9-12% of the
             interindividual variability in reward-related VS reactivity.
             In contrast, genetic variation directly affecting DA
             signaling only in the prefrontal cortex (COMT Val158Met) was
             not associated with variability in VS reactivity. Our
             results highlight an important role for genetic
             polymorphisms affecting striatal DA neurotransmission in
             mediating interindividual differences in reward-related VS
             reactivity. They further suggest that altered VS reactivity
             may represent a key neurobiological pathway through which
             these polymorphisms contribute to variability in behavioral
             impulsivity and related risk for substance use disorders. ©
             2009 Nature Publishing Group All rights reserved.},
   Language = {eng},
   Doi = {10.1038/sj.mp.4002086},
   Key = {Forbes2009b}
}

@article{Drabant2009,
   Author = {Drabant, EM and McRae, K and Manuck, SB and Hariri, AR and Gross,
             JJ},
   Title = {Individual Differences in Typical Reappraisal Use Predict
             Amygdala and Prefrontal Responses},
   Journal = {Biological Psychiatry},
   Volume = {65},
   Number = {5},
   Pages = {367-373},
   Address = {Department of Psychology, Stanford University, Stanford,
             California 94305, USA.},
   Year = {2009},
   ISSN = {0006-3223},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/18930182},
   Keywords = {Adult • Amygdala/*physiology •
             Emotions/*physiology • Facial Expression • Female
             • Humans • *Individuality • Middle Aged
             • Prefrontal Cortex/*physiology},
   Abstract = {Background: Participants who are instructed to use
             reappraisal to downregulate negative emotion show decreased
             amygdala responses and increased prefrontal responses.
             However, it is not known whether individual differences in
             the tendency to use reappraisal manifests in similar neural
             responses when individuals are spontaneously confronted with
             negative situations. Such spontaneous emotion regulation
             might play an important role in normal and pathological
             responses to the emotional challenges of everyday life.
             Methods: Fifty-six healthy women completed a blood
             oxygenation-level dependent functional magnetic resonance
             imaging challenge paradigm involving the perceptual
             processing of emotionally negative facial expressions.
             Participants also completed measures of typical emotion
             regulation use, trait anxiety, and neuroticism. Results:
             Greater use of reappraisal in everyday life was related to
             decreased amygdala activity and increased prefrontal and
             parietal activity during the processing of negative
             emotional facial expressions. These associations were not
             attributable to variation in trait anxiety, neuroticism, or
             the use of another common form of emotion regulation, namely
             suppression. Conclusions: These findings suggest that, like
             instructed reappraisal, individual differences in
             reappraisal use are associated with decreased activation in
             ventral emotion generative regions and increased activation
             in prefrontal control regions in response to negative
             stimuli. Such individual differences in emotion regulation
             might predict successful coping with emotional challenges as
             well as the onset of affective disorders. © 2009 Society of
             Biological Psychiatry.},
   Language = {eng},
   Doi = {10.1016/j.biopsych.2008.09.007},
   Key = {Drabant2009}
}

@article{Munoz2009,
   Author = {Muńoz, KE and Hyde, LW and Hariri, AR},
   Title = {Imaging genetics},
   Journal = {Journal of the American Academy of Child and Adolescent
             Psychiatry},
   Volume = {48},
   Number = {4},
   Pages = {356-361},
   Address = {Department of Psychology, Center for the Neural Basis of
             Cognition, University of Pittsburgh, Pittsburgh, PA
             15213-2593, USA.},
   Year = {2009},
   ISSN = {0890-8567},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/19318879},
   Keywords = {Amygdala/metabolism • Environment • Gene
             Expression/genetics • Genetic Predisposition to Disease
             • Heterozygote Detection/*instrumentation • Humans
             • Mental Disorders/*genetics/metabolism •
             Molecular Biology/*methods • Serotonin/genetics •
             Temperament},
   Language = {eng},
   Doi = {10.1097/CHI.0b013e31819aad07},
   Key = {Munoz2009}
}

@article{Gianaros2009,
   Author = {Gianaros, PJ and Hariri, AR and Sheu, LK and Muldoon, MF and Sutton-Tyrrell, K and Manuck, SB},
   Title = {Preclinical Atherosclerosis Covaries with Individual
             Differences in Reactivity and Functional Connectivity of the
             Amygdala},
   Journal = {Biological Psychiatry},
   Volume = {65},
   Number = {11},
   Pages = {943-950},
   Address = {Department of Psychiatry and Psychology, University of
             Pittsburgh, 3811 O'Hara Street, Pittsburgh, Pennsylvania
             15213, USA. gianarospj@upmc.edu},
   Year = {2009},
   ISSN = {0006-3223},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/19013557},
   Keywords = {Adult • Amygdala/blood supply/*physiopathology •
             Atherosclerosis/epidemiology/*pathology • Brain Mapping
             • Carotid Arteries/pathology • Female •
             Humans • Image Processing, Computer-Assisted/methods
             • *Individuality • Magnetic Resonance
             Imaging/methods • Male • Middle Aged •
             Oxygen/blood • Risk Factors • Statistics as Topic
             • Tunica Media/*pathology • Ultrasonography},
   Abstract = {Background: Cardiovascular disease (CVD) is a major source
             of medical comorbidity for patients with mood and anxiety
             disorders, and it remains the leading public health burden
             for the general population in industrialized nations.
             Indirect neurobiological evidence suggests that preclinical
             risk for atherosclerosis, the main contributor to CVD, may
             be conferred by interindividual variation in the
             functionality of the amygdala, a brain system jointly
             involved in processing behaviorally salient stimuli and
             regulating the cardiovascular system. Methods: In a
             neuroimaging study of 36 middle-aged adults (18 women) who
             were screened for confounding clinical cardiovascular and
             psychiatric disorders, we examined the direct covariation
             between a marker of preclinical atherosclerosis, carotid
             artery intima-media thickness (IMT), and interindividual
             variation in amygdala reactivity and functional connectivity
             assessed during the processing of behaviorally salient
             stimuli (angry and fearful facial expressions). Results:
             After accounting for traditional CVD risk factors, a
             thickening of carotid IMT across individuals covaried with
             greater amygdala reactivity and a more positive functional
             connectivity between the amygdala and perigenual anterior
             cingulate cortex, a corticolimbic area also implicated in
             behavioral salience processing and cardiovascular
             regulation. Conclusions: Individual differences in amygdala
             reactivity and functional connectivity may reflect facets of
             a novel, systems-level neural phenotype conferring risk for
             atherosclerosis and CVD. © 2009 Society of Biological
             Psychiatry.},
   Language = {eng},
   Doi = {10.1016/j.biopsych.2008.10.007},
   Key = {Gianaros2009}
}

@article{Forbes2009a,
   Author = {Forbes, EE and Hariri, AR and Martin, SL and Silk, JS and Moyles, DL and Fisher, PM and Brown, SM and Ryan, ND and Birmaher, B and Axelson, DA and Dahl, RE},
   Title = {Altered striatal activation predicting real-world positive
             affect in adolescent major depressive disorder},
   Journal = {American Journal of Psychiatry},
   Volume = {166},
   Number = {1},
   Pages = {64-73},
   Address = {University of Pittsburgh School of Medicine, Western
             Psychiatric Institute and Clinic, 3811 O'Hara St., Loeffler
             319, Pittsburgh, PA 15213, USA. forbese@upmc.edu},
   Year = {2009},
   ISSN = {0002-953X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/19047324},
   Keywords = {Adolescent • Affect/*physiology • Age Factors
             • Caudate Nucleus/physiopathology • Child •
             Computers, Handheld • Corpus Striatum/*physiopathology
             • Depressive Disorder, Major/diagnosis/*physiopathology/psychology
             • Dominance, Cerebral/physiology • Female •
             Humans • *Image Processing, Computer-Assisted •
             *Magnetic Resonance Imaging • Male • Motivation
             • Neurons/physiology • Oxygen/*blood •
             Prefrontal Cortex/physiopathology • Prognosis •
             Reward • *Social Environment},
   Abstract = {Objective: Alterations in reward-related brain function and
             phenomenological aspects of positive affect are increasingly
             examined in the development of major depressive disorder.
             The authors tested differences in reward-related brain
             function in healthy and depressed adolescents, and the
             authors examined direct links between reward-related brain
             function and positive mood that occurred in real-world
             contexts. Method: Fifteen adolescents with major depressive
             disorder and 28 adolescents with no history of psychiatric
             disorder, ages 8-17 years, completed a functional magnetic
             resonance imaging guessing task involving monetary reward.
             Participants also reported their subjective positive affect
             in natural environments during a 4-day cell-phone-based
             ecological momentary assessment. Results: Adolescents with
             major depressive disorder exhibited less striatal response
             than healthy comparison adolescents during reward
             anticipation and reward outcome, but more response in
             dorsolateral and medial prefrontal cortex. Diminished
             activation in a caudate region associated with this
             depression group difference was correlated with lower
             subjective positive affect in natural environments,
             particularly within the depressed group. Conclusions:
             Results support models of altered reward processing and
             related positive affect in young people with major
             depressive disorder and indicate that depressed adolescents'
             brain response to monetary reward is related to their
             affective experience in natural environments. Additionally,
             these results suggest that reward-processing paradigms
             capture brain function relevant to real-world positive
             affect.},
   Language = {eng},
   Doi = {10.1176/appi.ajp.2008.07081336},
   Key = {Forbes2009a}
}

@article{Fakra2009,
   Author = {Fakra, E and Hyde, LW and Gorka, A and Fisher, PM and Muñoz, KE and Kimak,
             M and Halder, I and Ferrell, RE and Manuck, SB and Hariri,
             AR},
   Title = {Effects of HTR1A C(-1019)G on amygdala reactivity and trait
             anxiety},
   Journal = {Archives of General Psychiatry},
   Volume = {66},
   Number = {1},
   Pages = {33-40},
   Address = {Hopital de laTimone, ServiceHospitalo-Universitaire
             dePsychiatrie, Hopital SteMarguerite, Marseille,
             France.},
   Year = {2009},
   ISSN = {0003-990X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/19124686},
   Keywords = {Adult • *Alleles • Amygdala/*physiopathology
             • Anger/physiology • Anxiety Disorders/*genetics/physiopathology
             • Arousal/*genetics/physiology •
             Attention/physiology • Autoreceptors/*genetics •
             Dominance, Cerebral/physiology • Facial Expression
             • Fear/physiology • Female • Genotype •
             Humans • *Image Processing, Computer-Assisted •
             *Magnetic Resonance Imaging • Male • Middle Aged
             • Oxygen/*blood • Pattern Recognition,
             Visual/physiology • Receptor, Serotonin,
             5-HT1A/*genetics • Signal Transduction/genetics},
   Abstract = {Context: Serotonin 1A (5-hydroxytryptamine 1A [5-HT1A])
             autoreceptors mediate negative feedback inhibition of
             serotonergic neurons and play a critical role in regulating
             serotonin signaling involved in shaping the functional
             response of major forebrain targets, such as the amygdala,
             supporting complex behavioral processes. A common functional
             variation (C[-1019]G) in the human 5-HT1A gene (HTR1A)
             represents 1 potential source of such interindi-vidual
             variability. Both in vitro and in vivo, -1019G blocks
             transcriptional repression, leading to increased
             autorecep-tor expression. Thus, -1019G may contribute to
             relatively decreased serotonin signaling at postsynaptic
             fore-brain target sites via increased negative feedback.
             Objectives: To evaluate the effects of HTR1A C(-1019)G on
             amygdala reactivity and to use path analyses to explore the
             impact of HTR1A-mediated variability in amygdala reactivity
             on individual differences in trait anxiety. We hypothesized
             that -1019G, which potentially results in decreased
             serotonin signaling, would be associated with relatively
             decreased amygdala reactivity and related trait anxiety.
             Design: Imaging genetics in participants from an archival
             database.Participants: Eighty-nine healthy adults. Results:
             Consistent with prior findings, -1019G was associated with
             significantly decreased threat-related amygdala reactivity.
             Importantly, this effect was independent of that associated
             with another common functional polymorphism that affects
             serotonin signaling, 5-HTTLPR. While there were no direct
             genotype effects on trait anxiety, HTR1A C(-1019)G
             indirectly predicted 9.2% of in-terindividual variability in
             trait anxiety through its effects on amygdala reactivity.
             Conclusions: Our findings further implicate relatively
             increased serotonin signaling, associated with a genetic
             variation that mediates increased 5-HT 1A autoreceptors, in
             driving amygdala reactivity and trait anxiety. Moreover,
             they provide empirical documentation of the basic premise
             that genetic variation indirectly affects emergent
             behavioral processes related to psychiatric disease risk by
             biasing the response of underlying neural circuitries. ©
             2009 American Medical Association.},
   Language = {eng},
   Doi = {10.1001/archpsyc.66.1.33},
   Key = {Fakra2009}
}

@article{Hariri2009b,
   Author = {Hariri, AR},
   Title = {The neurobiology of individual differences in complex
             behavioral traits},
   Journal = {Annual Review of Neuroscience},
   Volume = {32},
   Pages = {225-247},
   Address = {Department of Psychology and Neuroscience, Institute for
             Genome Sciences and Policy, Duke University, Durham, North
             Carolina 27708, USA. ah154@duke.edu},
   Year = {2009},
   ISSN = {0147-006X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/19400720},
   Keywords = {Animals • Behavior/*physiology • Biological
             Markers/analysis • Brain Mapping/*methods •
             Genetic Predisposition to Disease/genetics • Genetic
             Variation/physiology • Humans • Magnetic Resonance
             Imaging/*methods • Neuropsychology/*methods •
             Positron-Emission Tomography/*methods • *Quantitative
             Trait, Heritable},
   Abstract = {Neuroimaging, especially BOLD fMRI, has begun to identify
             how variability in brain function contributes to individual
             differences in complex behavioral traits. In parallel,
             pharmacological fMRI and multimodal PET/fMRI are identifying
             how variability in molecular signaling pathways influences
             individual differences in brain function. Against this
             background, functional genetic polymorphisms are being
             utilized to understand the origins of variability in
             signaling pathways as well as to model efficiently how such
             emergent variability impacts behaviorally relevant brain
             function. This article provides an overview of a research
             strategy seeking to integrate these complementary
             technologies and utilizes existing empirical data to
             illustrate its effectiveness in illuminating the
             neurobiology of individual differences in complex behavioral
             traits. The article also discusses how such efforts can
             contribute to the identification of predictive markers that
             interact with environmental factors to precipitate disease
             and to develop more effective and individually tailored
             treatment regimes. Copyright © 2009 by Annual Reviews. All
             rights reserved.},
   Language = {eng},
   Doi = {10.1146/annurev.neuro.051508.135335},
   Key = {Hariri2009b}
}

@article{Rasetti2009,
   Author = {Rasetti, R and Mattay, VS and Wiedholz, LM and Kolachana, BS and Hariri,
             AR and Callicott, JH and Meyer-Lindenberg, A and Weinberger,
             DR},
   Title = {Evidence that altered amygdala activity in schizophrenia is
             related to clinical state and not genetic
             risk},
   Journal = {American Journal of Psychiatry},
   Volume = {166},
   Number = {2},
   Pages = {216-225},
   Address = {Genes, Cognition, and Psychosis Program, IRP, NIMH, NIH, Rm.
             4S-235, 10 Center Dr., Bethesda, MD 20892,
             USA.},
   Year = {2009},
   ISSN = {0002-953X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/19074979},
   Keywords = {Adult • Amygdala/*physiopathology • Anger •
             Cognition Disorders/diagnosis/*genetics/*physiopathology
             • Dominance, Cerebral/physiology • Facial
             Expression • Fear/physiology • Female •
             Genetic Predisposition to Disease/*genetics • Gyrus
             Cinguli/physiopathology • Humans • *Image
             Processing, Computer-Assisted • Imaging,
             Three-Dimensional • *Magnetic Resonance Imaging •
             Male • Memory, Short-Term • Nerve
             Net/physiopathology • *Neuropsychological Tests •
             Oxygen/*blood • Pattern Recognition, Visual/physiology
             • Phenotype • Schizophrenia/diagnosis/*genetics/*physiopathology},
   Abstract = {Objective: Although amygdala dysfunction is reported in
             schizophrenia, it is unknown whether this deficit represents
             a heritable phenotype that is related to risk for
             schizophrenia or whether it is related to disease state. The
             purpose of the present study was to examine amygdala
             response to threatening faces among healthy siblings of
             schizophrenia patients in whom a subtler heritable deficit
             might be observed. Method: Participants were 34
             schizophrenia patients, 29 unaffected siblings, and 20
             healthy comparison subjects. Blood-oxygen-level-dependent
             (BOLD) functional magnetic resonance imaging (fMRI) was
             conducted during an implicit facial information processing
             task. The Nback working memory task, which has been shown to
             elicit prefrontal cortex abnormalities in unaffected
             siblings of schizophrenia patients, was employed as a
             positive experimental control. Results: Schizophrenia
             patients demonstrated a deficit in amygdala reactivity to
             negative face stimuli and an alteration, correlated with
             neuroleptic drug dosage, in the functional coupling between
             the amygdala and subgenual cingulate. In contrast,
             unaffected siblings showed a pattern that was not
             statistically different from that of healthy comparison
             subjects. During the N-back working memory task, both
             schizophrenia patients and their unaffected siblings
             demonstrated a pattern of inefficient prefrontal cortex
             engagement, which is consistent with earlier evidence that
             this pattern is related to genetic risk for schizophrenia.
             Conclusions: These data suggest that the pathophysiological
             mechanism underlying the inability of individuals with
             schizophrenia to normally engage the amygdala in processing
             fearful and angry facial representations is more likely a
             phenomenon related to the disease state, specifically to
             treatment.},
   Language = {eng},
   Doi = {10.1176/appi.ajp.2008.08020261},
   Key = {Rasetti2009}
}

@article{Fisher2009,
   Author = {Fisher, PM and Meltzer, CC and Price, JC and Coleman, RL and Ziolko, SK and Becker, C and Moses-Kolko, EL and Berga, SL and Hariri,
             AR},
   Title = {Medial prefrontal cortex 5-HT2A density is
             correlated with amygdala reactivity, response habituation,
             and functional coupling},
   Journal = {Cerebral Cortex},
   Volume = {19},
   Number = {11},
   Pages = {2499-2507},
   Address = {Center for Neuroscience, University of Pittsburgh,
             Pittsburgh, PA 15213, USA.},
   Year = {2009},
   ISSN = {1047-3211},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/19321655},
   Keywords = {Adult • Amygdala/*physiology •
             Emotions/*physiology • Female • Habituation,
             Psychophysiologic/*physiology • Humans • Male
             • Neural Inhibition/*physiology • Prefrontal
             Cortex/*physiology • Receptor, Serotonin,
             5-HT2A/*metabolism • Tissue Distribution},
   Abstract = {Feedback inhibition of the amygdala via medial prefrontal
             cortex (mPFC) is an important component in the regulation of
             complex emotional behaviors. The functional dynamics of this
             corticolimbic circuitry are, in part, modulated by serotonin
             (5-HT). Serotonin 2A (5-HT2A) receptors within the mPFC
             represent a potential molecular mechanism through which 5-HT
             can modulate this corticolimbic circuitry. We employed a
             multimodal neuroimaging strategy to explore the relationship
             between threat-related amygdala reactivity, assessed using
             blood oxygen level-dependent functional magnetic resonance
             imaging, and mPFC 5-HT2A density, assessed using
             [18F]altanserin positron emission tomography in 35 healthy
             adult volunteers. We observed a significant inverse
             relationship wherein greater mPFC 5-HT2A density was
             associated with reduced threat-related right amygdala
             reactivity. Remarkably, 25-37% of the variability in
             amygdala reactivity was explained by mPFC 5-HT2A density. We
             also observed a positive correlation between mPFC 5-HT2A
             density and the magnitude of right amygdala habituation.
             Furthermore, functional coupling between the amygdala and
             mPFC was positively correlated with 5-HT2A density
             suggesting that effective integration of emotionally salient
             information within this corticolimbic circuitry may be
             modulated, at least in part, by mPFC 5-HT2A. Collectively,
             our results indicate that mPFC 5-HT2A is strongly associated
             with threat-related amygdala reactivity as well as its
             temporal habituation and functional coupling with prefrontal
             regulatory regions.},
   Language = {eng},
   Doi = {10.1093/cercor/bhp022},
   Key = {Fisher2009}
}

@article{Hariri2009a,
   Author = {Hariri, AR and Gorka, A and Hyde, LW and Kimak, M and Halder, I and Ducci,
             F and Ferrell, RE and Goldman, D and Manuck, SB},
   Title = {Divergent Effects of Genetic Variation in Endocannabinoid
             Signaling on Human Threat- and Reward-Related Brain
             Function},
   Journal = {Biological Psychiatry},
   Volume = {66},
   Number = {1},
   Pages = {9-16},
   Address = {Department of Psychiatry, University of Pittsburgh,
             Pittsburgh, Pennsylvania 15213, USA. haririar@upmc.edu},
   Year = {2009},
   ISSN = {0006-3223},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/19103437},
   Keywords = {Adult • Amidohydrolases/*genetics • Analysis of
             Variance • Anxiety/*genetics • Brain/anatomy \&
             histology/blood supply/*physiology • Brain Mapping
             • Cannabinoid Receptor Modulators/genetics •
             Endocannabinoids • Female • Genetic
             Variation/*genetics • Genotype • Humans •
             Image Processing, Computer-Assisted/methods • Magnetic
             Resonance Imaging/methods • Male • Middle Aged
             • Oxygen/blood • Psychiatric Status Rating Scales
             • Regression Analysis • *Reward • *Signal
             Transduction/genetics},
   Abstract = {Background: Fatty acid amide hydrolase (FAAH) is a key
             enzyme in regulating endocannabinoid (eCB) signaling. A
             common single nucleotide polymorphism (C385A) in the human
             FAAH gene has been associated with increased risk for
             addiction and obesity. Methods: Using imaging genetics in 82
             healthy adult volunteers, we examined the effects of FAAH
             C385A on threat- and reward-related human brain function.
             Results: Carriers of FAAH 385A, associated with reduced
             enzyme and possibly increased eCB signaling, had decreased
             threat-related amygdala reactivity but increased
             reward-related ventral striatal reactivity in comparison
             with C385 homozygotes. Similarly divergent effects of FAAH
             C385A genotype were manifest at the level of brain-behavior
             relationships. The 385A carriers showed decreased
             correlation between amygdala reactivity and trait anxiety
             but increased correlation between ventral striatal
             reactivity and delay discounting, an index of impulsivity.
             Conclusions: Our results parallel pharmacologic and genetic
             dissection of eCB signaling, are consistent with the
             psychotropic effects of Δ9-tetrahydrocannabinol, and
             highlight specific neural mechanisms through which
             variability in eCB signaling impacts complex behavioral
             processes related to risk for addiction and obesity. © 2009
             Society of Biological Psychiatry.},
   Language = {eng},
   Doi = {10.1016/j.biopsych.2008.10.047},
   Key = {Hariri2009a}
}

@article{Krystal2008,
   Author = {Krystal, JH and Carter, CS and Geschwind, D and Manji, HK and March, JS and Nestler, EJ and Zubieta, J-K and Charney, DS and Goldman, D and Gur, RE and Lieberman, JA and Roy-Byrne, P and Rubinow, DR and Anderson, SA and Barondes, S and Berman, KF and Blair, J and Braff, DL and Brown, ES and Calabrese, JR and Carlezon, WA and Cook, EH and Davidson, RJ and Davis,
             M and Desimone, R and Drevets, WC and Duman, RS and Essock, SM and Faraone,
             SV and Freedman, R and Friston, KJ and Gelernter, J and Geller, B and Gill,
             M and Gould, E and Grace, AA and Grillon, C and Gueorguieva, R and Hariri,
             AR and Innis, RB et al.},
   Title = {It is time to take a stand for medical research and against
             terrorism targeting medical scientists.},
   Journal = {Biological Psychiatry},
   Volume = {63},
   Number = {8},
   Pages = {725-727},
   Address = {Department of Psychiatry, Yale University School of
             Medicine, New Haven, Connecticut, USA. john.krystal@yale.edu},
   Year = {2008},
   Month = {April},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/18371494},
   Keywords = {*Animal Experimentation • Animal Rights • Animals
             • *Attitude of Health Personnel • *Biomedical
             Research • Crime/prevention \& control • Ethics,
             Research • Humans • Primates • *Research
             Personnel • Terrorism/*prevention \& control •
             United States},
   Language = {eng},
   Doi = {10.1016/j.biopsych.2008.03.005},
   Key = {Krystal2008}
}

@article{fds251999,
   Author = {Hariri, AR},
   Title = {Imaging genetics offers new predictive markers of individual
             differences in behavior and risk for psychiatric
             diseases},
   Journal = {Neuropsychopharmacology (Nature)},
   Volume = {33},
   Number = {1},
   Pages = {201-202},
   Year = {2008},
   ISSN = {0893-133X},
   url = {http://dx.doi.org/10.1038/sj.npp.1301608},
   Doi = {10.1038/sj.npp.1301608},
   Key = {fds251999}
}

@article{fds252000,
   Author = {Pezawas, L and Meyer-Lindenberg, A and Goldman, AL and Verchinski,
             BA and Chen, G and Kolachana, BS and Egan, MF and Mattay, VS and Hariri,
             AR and Weinberger, DR},
   Title = {MET BDNF protects against morphological S allele effects of
             5-HTTLPR},
   Journal = {Molecular Psychiatry},
   Volume = {13},
   Number = {7},
   Pages = {654-},
   Year = {2008},
   ISSN = {1359-4184},
   url = {http://dx.doi.org/10.1038/mp.2008.61},
   Doi = {10.1038/mp.2008.61},
   Key = {fds252000}
}

@article{Gianaros2008b,
   Author = {Gianaros, PJ and Horenstein, JA and Hariri, AR and Sheu, LK and Manuck,
             SB and Matthews, KA and Cohen, S},
   Title = {Potential neural embedding of parental social
             standing},
   Journal = {Social Cognitive and Affective Neuroscience},
   Volume = {3},
   Number = {2},
   Pages = {91-96},
   Address = {Department of Psychiatry, University of Pittsburgh, 3811
             O'Hara Street, Pittsburgh, PA 15213, USA.
             gianarospj@upmc.edu},
   Year = {2008},
   ISSN = {1749-5016},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/18594696},
   Keywords = {Adaptation, Psychological/physiology •
             Aggression/*physiology/psychology •
             Amygdala/*physiology • Facial Expression •
             Hierarchy, Social • Humans • Magnetic Resonance
             Imaging • Male • Parents/psychology •
             Reference Values • Self Concept • *Social Class
             • *Social Perception • Stress,
             Psychological/*physiopathology • Young
             Adult},
   Abstract = {Socioeconomic disadvantage during childhood and adolescence
             predicts poor mental and physical health and premature death
             by major medical diseases in adulthood. However, the neural
             pathways through which socioeconomic factors may exert a
             developmental influence on health and longevity remain
             largely unknown. This fMRI study provides novel evidence of
             a unique relationship between the perception that one's
             parents had a relatively low social standing-a putative
             indicator of early socioeconomic disadvantage- and greater
             amygdala reactivity to threatening facial expressions. This
             relationship was not explained by several possible
             confounders, including sex, ethnicity, dispositional
             emotionality, symptoms of depression and anxiety, parental
             education and participants' perceptions of their own social
             standing. The amygdala expresses marked developmental
             plasticity and plays instrumental roles in processing
             emotional information, regulating emotion-related behaviors
             and orchestrating biobehavioral stress responses throughout
             life. Thus, these findings may provide insight into the
             neurodevelopmental pathways impacting socioeconomic
             disparities in health. © The Author (2008). Published by
             Oxford University Press.},
   Language = {eng},
   Doi = {10.1093/scan/nsn003},
   Key = {Gianaros2008b}
}

@article{Fisher2008,
   Author = {Fisher, PM and Muñoz, KE and Hariri, AR},
   Title = {Identification of neurogenetic pathways of risk for
             psychopathology},
   Journal = {American Journal of Medical Genetics Part C: Seminars in
             Medical Genetics},
   Volume = {148},
   Number = {2},
   Pages = {147-153},
   Address = {University of Pittsburgh, Pittsburgh, PA 15213-2593,
             USA.},
   Year = {2008},
   ISSN = {1552-4868},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/18412103},
   Keywords = {Brain/growth \& development/*physiopathology • Catechol
             O-Methyltransferase/genetics/physiology • Diagnostic
             Imaging • Dopamine Plasma Membrane Transport
             Proteins/genetics/physiology • Female • Humans
             • Male • Mental Disorders/diagnosis/*genetics/*physiopathology
             • Monoamine Oxidase/genetics/physiology •
             Psychopathology • Risk Factors • Serotonin Plasma
             Membrane Transport Proteins/genetics/physiology •
             Tryptophan Hydroxylase/genetics/physiology},
   Abstract = {Imaging genetics has been a highly effective and
             increasingly applied strategy for identifying the impact of
             genetic polymorphisms on individual differences in neural
             circuitry supporting complex behaviors. The application of
             imaging genetics towards further elucidating neural
             circuitry associated with the pathophysiology of psychiatric
             illness is of particular interest given its potential to
             guide the development and improvement of current therapeutic
             methods. The identification of genetic variants that
             contribute to or predict the disruption of specific neural
             pathways associated with psychopathology may also serve as
             useful markers of risk demarcating individuals with elevated
             susceptibility for psychiatric illness and affording early
             or even preemptive treatment strategies. In the continued
             development of this technique, recent multimodal
             neuroimaging strategies and studies examining the effects of
             multiple genes in concert within large subject populations
             have shown promise in the development of a more complete
             understanding of the interrelationships between genes, brain
             function, behavior and associated risk for psychopathology.
             © 2008 Wiley-Liss, Inc.},
   Language = {eng},
   Doi = {10.1002/ajmg.c.30173},
   Key = {Fisher2008}
}

@article{Munafo2008,
   Author = {Munafò, MR and Brown, SM and Hariri, AR},
   Title = {Serotonin Transporter (5-HTTLPR) Genotype and Amygdala
             Activation: A Meta-Analysis},
   Journal = {Biological Psychiatry},
   Volume = {63},
   Number = {9},
   Pages = {852-857},
   Address = {Department of Experimental Psychology, University of
             Bristol, United Kingdom. marcus.munafo@bristol.ac.uk},
   Year = {2008},
   ISSN = {0006-3223},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/17949693},
   Keywords = {Adolescent • Adult • Alleles •
             Amygdala/*physiopathology • Anxiety
             Disorders/genetics/physiopathology • Depressive
             Disorder/genetics/physiopathology • Female •
             *Genotype • Humans • Individuality • Magnetic
             Resonance Imaging • Male • Phenotype •
             Polymorphism, Genetic/*genetics • Promoter Regions,
             Genetic/*genetics • Serotonin Plasma Membrane Transport
             Proteins/*genetics • Stress, Psychological/complications},
   Abstract = {Background: We evaluated the magnitude of the reported
             associations between amygdala activation and the serotonin
             transporter gene linked polymorphic region (5-HTTLPR) and
             the likely effect size of this relationship. Methods: We
             used meta-analytic techniques to combine data from existing
             published and unpublished studies. We also tested for
             possible publication bias and explored possible moderating
             influences on any association, such as sample ancestry.
             Results: Our results provide support for the association of
             the 5-HTTLPR polymorphism and amygdala activation and
             suggest that this locus may account for up to 10% of
             phenotypic variance. Although we did not observe evidence
             for potential publication bias in our main analysis, this
             was due in part to efforts to obtain unpublished data
             pertinent to this meta-analysis, and when three unpublished
             data sets were excluded we did observe evidence of such
             bias. We also observed evidence that the first published
             study may provide an overestimate of the true effect size,
             which is consistent with findings from genetic association
             studies of other phenotypes. Conclusions: Although our
             analysis provides support for the association of the
             5-HTTLPR polymorphism and amygdala activation, it also
             suggests that most studies to date are nevertheless lacking
             in statistical power. Increasing the sample sizes of future
             imaging genetics studies will allow a more accurate
             characterization of any true effect size and afford adequate
             power to examine the impact of multiple polymorphisms that
             likely work in concert to affect gene function and, in turn,
             bias neural processes mediating dispositional traits such as
             temperament and personality. © 2008 Society of Biological
             Psychiatry.},
   Language = {eng},
   Doi = {10.1016/j.biopsych.2007.08.016},
   Key = {Munafo2008}
}

@article{Ousdal2008,
   Author = {Ousdal, OT and Jensen, J and Server, A and Hariri, AR and Nakstad, PH and Andreassen, OA},
   Title = {The human amygdala is involved in general behavioral
             relevance detection: Evidence from an event-related
             functional magnetic resonance imaging Go-NoGo
             task},
   Journal = {Neuroscience},
   Volume = {156},
   Number = {3},
   Pages = {450-455},
   Address = {TOP Project, Psychosis Research Section, Division of
             Psychiatry, Building 49, Ulleval University Hospital, Oslo,
             Norway.},
   Year = {2008},
   ISSN = {0306-4522},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/18775476},
   Keywords = {Adult • Amygdala/*blood supply/*physiology •
             Decision Making/*physiology • Female • Humans
             • Image Processing, Computer-Assisted • *Magnetic
             Resonance Imaging • Male • Neuropsychological
             Tests • Oxygen/blood • Pattern Recognition, Visual
             • Photic Stimulation/methods • Reaction
             Time/physiology • Signal Detection,
             Psychological/*physiology • Young Adult},
   Abstract = {The amygdala is classically regarded as a detector of
             potential threat and as a critical component of the neural
             circuitry mediating conditioned fear responses. However, it
             has been reported that the human amygdala responds to
             multiple expressions of emotions as well as emotionally
             neutral stimuli of a novel, uncertain or ambiguous nature.
             Thus, it has been proposed that the function of the amygdala
             may be of a more general art, i.e. as a detector of
             behaviorally relevant stimuli [Sander D, Grafman J, Zalla T
             (2003) The human amygdala: an evolved system for relevance
             detection. Rev Neurosci 14:303-316]. To investigate this
             putative function of the amygdala, we used event related
             functional magnetic resonance imaging (fMRI) and a modified
             Go-NoGo task composed of behaviorally relevant and
             irrelevant letter and number stimuli. Analyses revealed
             bilateral amygdala activation in response to letter stimuli
             that were behaviorally relevant as compared with letters
             with less behavioral relevance. Similar results were
             obtained for relatively infrequent NoGo relevant stimuli as
             compared with more frequent Go stimuli. Our findings support
             a role for the human amygdala in general detection of
             behaviorally relevant stimuli. © 2008 IBRO.},
   Language = {eng},
   Doi = {10.1016/j.neuroscience.2008.07.066},
   Key = {Ousdal2008}
}

@article{Fakra2008,
   Author = {Fakra, E and Salgado-Pineda, P and Delaveau, P and Hariri, AR and Blin,
             O},
   Title = {Neural bases of different cognitive strategies for facial
             affect processing in schizophrenia},
   Journal = {Schizophrenia Research},
   Volume = {100},
   Number = {1-3},
   Pages = {191-205},
   Address = {CIC-UPCET, Hopital de la Timone, UMR CNRS 6193 INCM,
             Marseille, France. eric.fakra@ap-hm.fr},
   Year = {2008},
   ISSN = {0920-9964},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/18234477},
   Keywords = {Adult • Affect/*physiology • Amygdala/physiopathology
             • Brain/*physiopathology • Brain Mapping •
             Cerebral Cortex/physiopathology • Control Groups •
             *Facial Expression • Female • Functional
             Laterality/physiology • Humans • Limbic
             System/physiopathology • Magnetic Resonance
             Imaging/*statistics \& numerical data • Male •
             Models, Neurological • Neural Pathways/physiopathology
             • Recognition (Psychology)/physiology •
             Schizophrenia/*diagnosis/physiopathology •
             *Schizophrenic Psychology • Social Perception •
             Task Performance and Analysis • Visual
             Perception/*physiology},
   Abstract = {Objective: To examine the neural basis and dynamics of
             facial affect processing in schizophrenic patients as
             compared to healthy controls. Method: Fourteen schizophrenic
             patients and fourteen matched controls performed a facial
             affect identification task during fMRI acquisition. The
             emotional task included an intuitive emotional condition
             (matching emotional faces) and a more cognitively demanding
             condition (labeling emotional faces). Individual analysis
             for each emotional condition, and second-level t-tests
             examining both within-, and between-group differences, were
             carried out using a random effects approach.
             Psychophysiological interactions (PPI) were tested for
             variations in functional connectivity between amygdala and
             other brain regions as a function of changes in experimental
             conditions (labeling versus matching). Results: During the
             labeling condition, both groups engaged similar networks.
             During the matching condition, schizophrenics failed to
             activate regions of the limbic system implicated in the
             automatic processing of emotions. PPI revealed an inverse
             functional connectivity between prefrontal regions and the
             left amygdala in healthy volunteers but there was no such
             change in patients. Furthermore, during the matching
             condition, and compared to controls, patients showed
             decreased activation of regions involved in holistic face
             processing (fusiform gyrus) and increased activation of
             regions associated with feature analysis (inferior parietal
             cortex, left middle temporal lobe, right precuneus).
             Conclusions: Our findings suggest that schizophrenic
             patients invariably adopt a cognitive approach when
             identifying facial affect. The distributed neocortical
             network observed during the intuitive condition indicates
             that patients may resort to feature-based, rather than
             configuration-based, processing and may constitute a
             compensatory strategy for limbic dysfunction. © 2007
             Elsevier B.V. All rights reserved.},
   Language = {eng},
   Doi = {10.1016/j.schres.2007.11.040},
   Key = {Fakra2008}
}

@article{Pezawas2008,
   Author = {Pezawas, L and Meyer-Lindenberg, A and Goldman, AL and Verchinski,
             BA and Chen, G and Kolachana, BS and Egan, MF and Mattay, VS and Hariri,
             AR and Weinberger, DR},
   Title = {Evidence of biologic epistasis between BDNF and SLC6A4 and
             implications for depression},
   Journal = {Molecular Psychiatry},
   Volume = {13},
   Number = {7},
   Pages = {709-716},
   Address = {Genes, Cognition and Psychosis Program, National Institute
             of Mental Health, National Institutes of Health, Bethesda,
             MD 20892, USA.},
   Year = {2008},
   ISSN = {1359-4184},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/18347599},
   Keywords = {Amino Acid Substitution • Brain/pathology •
             Brain-Derived Neurotrophic Factor/*genetics •
             Depression/*genetics/pathology • Depressive
             Disorder/*genetics/pathology • *Epistasis, Genetic
             • European Continental Ancestry Group/genetics •
             Gyrus Cinguli/pathology • Humans • Magnetic
             Resonance Imaging • Polymorphism, Genetic •
             Reference Values • Serotonin Plasma Membrane Transport
             Proteins/*genetics},
   Abstract = {Complex genetic disorders such as depression likely exhibit
             epistasis, but neural mechanisms of such gene-gene
             interactions are incompletely understood. 5-HTTLPR and BDNF
             VAL66MET, functional polymorphisms of the serotonin (5-HT)
             transporter (SLC6A4) and brain-derived neurotrophic factor
             (BDNF) gene, impact on two distinct, but interacting
             signaling systems, which have been related to depression and
             to the modulation of neurogenesis and plasticity of
             circuitries of emotion processing. Recent clinical studies
             suggest that the BDNF MET allele, which shows abnormal
             intracellular trafficking and regulated secretion, has a
             protective effect regarding the development of depression
             and in mice of social defeat stress. Here we show, using
             anatomical neuroimaging techniques in a sample of healthy
             subjects (n=111), that the BDNF MET allele, which is
             predicted to have reduced responsivity to 5-HT signaling,
             protects against 5-HTTLPR S allele-induced effects on a
             brain circuitry encompassing the amygdala and the subgenual
             portion of the anterior cingulate (rAC). Our analyses
             revealed no effect of the 5-HTTLPR S allele on rAC volume in
             the presence of BDNF MET alleles, whereas a significant
             volume reduction (P&lt;0.001) was seen on BDNF VAL/VAL
             background. Interacting genotype effects were also found in
             structural connectivity between amygdala and rAC (P=0.002).
             These data provide in vivo evidence of biologic epistasis
             between SLC6A4 and BDNF in the human brain by identifying a
             neural mechanism linking serotonergic and neurotrophic
             signaling on the neural systems level, and have implications
             for personalized treatment planning in depression. © 2008
             Nature Publishing Group All rights reserved.},
   Language = {eng},
   Doi = {10.1038/mp.2008.32},
   Key = {Pezawas2008}
}

@article{Kienast2008,
   Author = {Kienast, T and Hariri, AR and Schlagenhauf, F and Wrase, J and Sterzer,
             P and Buchholz, HG and Smolka, MN and Gründer, G and Cumming, P and Kumakura, Y and Bartenstein, P and Dolan, RJ and Heinz,
             A},
   Title = {Dopamine in amygdala gates limbic processing of aversive
             stimuli in humans},
   Journal = {Nature Neuroscience},
   Volume = {11},
   Number = {12},
   Pages = {1381-1382},
   Address = {Department of Psychiatry and Psychotherapy, Campus Charite
             Mitte, Charite-University Medicine Berlin, Chariteplatz 1,
             10117 Berlin, Germany.},
   Year = {2008},
   ISSN = {1097-6256},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/18978778},
   Keywords = {Adult • *Affect • Amygdala/blood
             supply/*metabolism/radionuclide imaging • *Brain
             Mapping • Dihydroxyphenylalanine/analogs \&
             derivatives/pharmacokinetics • Dopamine/*metabolism
             • Fluorine Radioisotopes/pharmacokinetics • Gyrus
             Cinguli/blood supply/radionuclide imaging • Humans
             • Image Processing, Computer-Assisted • Limbic
             System/*metabolism/radionuclide imaging • Magnetic
             Resonance Imaging/methods • Male • Middle Aged
             • Oxygen/blood • Positron-Emission
             Tomography/methods • Psychophysics},
   Abstract = {Dopamine is released under stress and modulates processing
             of aversive stimuli. We found that dopamine storage capacity
             in human amygdala, measured with 6-[18F]fluoro-L-DOPA
             positron emission tomography, was positively correlated with
             functional magnetic resonance imaging blood oxygen
             level-dependent signal changes in amygdala and dorsal
             anterior cingulate cortex that were evoked by aversive
             stimuli. Furthermore, functional connectivity between these
             two regions was inversely related to trait anxiety. Our
             results suggest that individual dopamine storage capacity in
             amygdala subserves modulation of emotional processing in
             amygdala and dorsal cingulate, thereby contributing to
             individual differences in anxious temperament. © 2008
             Nature Publishing Group.},
   Language = {eng},
   Doi = {10.1038/nn.2222},
   Key = {Kienast2008}
}

@article{Zanardi2008,
   Author = {Zanardi, R and Barbini, B and Rossini, D and Bernasconi, A and Fregni,
             F and Padberg, F and Rossi, S and Wirz-Justice, A and Terman, M and Martiny, K and Bersani, G and Hariri, AR and Pezawas, L and Roiser, JP and Bertolino, A and Calabrese, G and Magri, L and Benedetti, F and Pontiggia, A and Malaguti, A and Smeraldi, E and Colombo,
             C},
   Title = {New perspectives on techniques for the clinical
             psychiatrist: Brain stimulation, chronobiology and
             psychiatric brain imaging},
   Journal = {Psychiatry and Clinical Neurosciences},
   Volume = {62},
   Number = {6},
   Pages = {627-637},
   Address = {San Raffaele Hospital Department of Psychiatry, Vita-Salute
             University, Milan, Italy. zanardi.raffaella@hsr.it},
   Year = {2008},
   ISSN = {1323-1316},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/19067998},
   Keywords = {Brain/*pathology • Diagnostic Imaging • Humans
             • Magnetic Resonance Imaging • Magnetic Resonance
             Spectroscopy • Mental Disorders/pathology/physiopathology/*therapy
             • Mood Disorders/psychology • Periodicity •
             Psychiatry/*methods/*trends • Tomography,
             Emission-Computed, Single-Photon • *Transcranial
             Magnetic Stimulation},
   Abstract = {This review summarizes a scientific dialogue between
             representatives in non-pharmacological treatment options of
             affective disorders. Among the recently introduced somatic
             treatments for depression those with most evidenced efficacy
             will be discussed. The first part of this article presents
             current opinions about the clinical applications of
             transcranial magnetic stimulation in the treatment of
             depression. The second part explains the most relevant uses
             of chronobiology in mood disorders, while the last part
             deals with the main perspectives on brain imaging techniques
             in psychiatry. The aim was to bridge gaps between the
             research evidence and clinical decisions, and reach an
             agreement on several key points of chronobiological and
             brain stimulation techniques, as well as on relevant
             objectives for future research. © 2008 The
             Authors.},
   Language = {eng},
   Doi = {10.1111/j.1440-1819.2008.01863.x},
   Key = {Zanardi2008}
}

@article{Marsland2008,
   Author = {Marsland, AL and Gianaros, PJ and Abramowitch, SM and Manuck, SB and Hariri, AR},
   Title = {Interleukin-6 Covaries Inversely with Hippocampal Grey
             Matter Volume in Middle-Aged Adults},
   Journal = {Biological Psychiatry},
   Volume = {64},
   Number = {6},
   Pages = {484-490},
   Address = {Behavioral Immunology Laboratory, University of Pittsburgh,
             PA 15260, USA. marsland@pitt.edu},
   Year = {2008},
   ISSN = {0006-3223},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/18514163},
   Keywords = {Adipose Tissue/metabolism • Adult • Cognition
             Disorders/diagnosis/epidemiology • Diagnostic and
             Statistical Manual of Mental Disorders • Female •
             Hippocampus/*anatomy \& histology/*metabolism • Humans
             • Hypertension/epidemiology/metabolism •
             Inflammation/epidemiology/metabolism •
             Interleukin-6/*metabolism • Magnetic Resonance Imaging
             • Male • Middle Aged • Nerve Net/metabolism
             • Registries • Severity of Illness Index •
             Wechsler Scales},
   Abstract = {Background: Converging animal findings suggest that higher
             peripheral levels of inflammation are associated with
             activation of central inflammatory mechanisms that result in
             hippocampal neurodegeneration and related impairment of
             memory function. We have recently shown, consistent with
             animal findings, an inverse association between peripheral
             levels of interleukin-6 (IL-6), a relatively stable marker
             of systemic inflammation, and memory function in mid-life
             adults. In the current study, we extend this work to test
             whether systemic inflammation is associated with reduced
             grey matter volume of the hippocampus. Methods: For this
             purpose, we used a computational structural neuroimaging
             method (optimized voxel-based morphometry) to evaluate the
             relationship between plasma IL-6 levels and hippocampal grey
             matter volume in a sample of 76 relatively healthy community
             volunteers ages 30-54. Results: Peripheral levels of IL-6
             covaried inversely with hippocampal grey matter volume, and
             this relationship persisted after accounting for several
             possible confounders, including age, gender, race, years of
             education, percent body fat, blood pressure, smoking,
             physical activity, hours of sleep, alcohol use, and total
             grey matter volume. Conclusions: To our knowledge, this is
             the first report of a relationship between a peripheral
             marker of IL-6 and hippocampal grey matter volume, raising
             the possibility that low-grade systemic inflammation could
             plausibly presage subclinical cognitive decline in part via
             structural neural pathways. © 2008 Society of Biological
             Psychiatry.},
   Language = {eng},
   Doi = {10.1016/j.biopsych.2008.04.016},
   Key = {Marsland2008}
}

@article{Buckholtz2008,
   Author = {Buckholtz, JW and Callicott, JH and Kolachana, B and Hariri, AR and Goldberg, TE and Genderson, M and Egan, MF and Mattay, VS and Weinberger, DR and Meyer-Lindenberg, A},
   Title = {Genetic variation in MAOA modulates ventromedial prefrontal
             circuitry mediating individual differences in human
             personality},
   Journal = {Molecular Psychiatry},
   Volume = {13},
   Number = {3},
   Pages = {313-324},
   Address = {Neuroimaging Core Facility, National Institute for Mental
             Health, NIH, DHHS, Bethesda, MD 20892-1365,
             USA.},
   Year = {2008},
   ISSN = {1359-4184},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/17519928},
   Keywords = {Adult • Brain Mapping • Facial Expression •
             Female • *Genetic Variation • Humans • Image
             Processing, Computer-Assisted • *Individuality •
             Magnetic Resonance Imaging • Male • Models,
             Biological • Monoamine Oxidase/*genetics • Neural
             Pathways/blood supply/physiology • Neuropsychological
             Tests • Oxygen/blood • Personality/*genetics
             • Photic Stimulation/methods • Prefrontal
             Cortex/blood supply/*physiology},
   Abstract = {Little is known about neural mechanisms underlying human
             personality and temperament, despite their considerable
             importance as highly heritable risk mediators for somatic
             and psychiatric disorders. To identify these circuits, we
             used a combined genetic and imaging approach focused on
             Monoamine Oxidase A (MAOA), encoding a key enzyme for
             monoamine metabolism previously associated with temperament
             and antisocial behavior. Male carriers of a low-expressing
             genetic variant exhibited dysregulated amygdala activation
             and increased functional coupling with ventromedial
             prefrontal cortex (vmPFC). Stronger coupling predicted
             increased harm avoidance and decreased reward dependence
             scores, suggesting that this circuitry mediates a part of
             the association of MAOA with these traits. We utilized path
             analysis to parse the effective connectivity within this
             system, and provide evidence that vmPFC regulates amygdala
             indirectly by influencing rostral cingulate cortex function.
             Our data implicate a neural circuit for variation in human
             personality under genetic control, provide an anatomically
             consistent mechanism for vmPFC-amygdala interactions
             underlying this variation, and suggest a role for vmPFC as a
             superordinate regulatory area for emotional arousal and
             social behavior. © 2008 Nature Publishing Group All rights
             reserved.},
   Language = {eng},
   Doi = {10.1038/sj.mp.4002020},
   Key = {Buckholtz2008}
}

@article{Bigos2008,
   Author = {Bigos, KL and Pollock, BG and Aizenstein, HJ and Fisher, PM and Bies,
             RR and Hariri, AR},
   Title = {Acute 5-HT reuptake blockade potentiates human amygdala
             reactivity},
   Journal = {Neuropsychopharmacology (Nature)},
   Volume = {33},
   Number = {13},
   Pages = {3221-3225},
   Address = {Department of Pharmaceutical Sciences, University of
             Pittsburgh, PA, USA. bigosk@mail.nih.gov},
   Year = {2008},
   ISSN = {0893-133X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/18463627},
   Keywords = {Adult • Akathisia, Drug-Induced/metabolism/physiopathology
             • Amygdala/*drug effects/*metabolism •
             Anxiety/chemically induced/metabolism/physiopathology •
             Brain Chemistry/*drug effects/*physiology •
             Citalopram/*pharmacology • Cross-Over Studies •
             Depressive Disorder/drug therapy/metabolism/physiopathology
             • Dose-Response Relationship, Drug • Double-Blind
             Method • Facial Expression • Humans • Male
             • Middle Aged • Neuropsychological Tests •
             Photic Stimulation • Presynaptic Terminals/drug
             effects/metabolism • Serotonin/*metabolism •
             Serotonin Uptake Inhibitors/pharmacology • Young
             Adult},
   Abstract = {Variability in serotonin (5-HT) function is associated with
             individual differences in normal mood and temperament, as
             well as psychiatric illnesses, all of which are influenced
             by amygdala function. This study evaluated the acute effects
             of 5-HT reuptake blockade on amygdala function using
             pharmacological functional MRI. Eight healthy men completed
             a double-blind balanced crossover study with the selective
             5-HT reuptake inhibitor, citalopram (20 mg infused over 30
             min), and normal saline. Amygdala reactivity in response to
             novel facial expressions was assessed on three successive
             scans, once before drug/placebo infusion, once early in the
             infusion, and once at the end of infusion. Acute citalopram
             administration resulted in concentration-dependent increases
             in human amygdala reactivity to salient stimuli. The current
             pattern of 5-HT-mediated amygdala reactivity may represent
             an important pathway through which SSRIs achieve an
             antidepressant effect. Intriguingly, our data may also
             reveal a mechanism contributing to clinical observations of
             extreme agitation, restlessness, and suicidal ideation in
             some individuals during acute SSRI treatment. Developing a
             comprehensive model of how 5-HT modulates human amygdala
             reactivity supporting behavioral and physiological arousal
             will be instrumental for our understanding of basic
             neurobehavioral processes, their dysfunction in psychiatric
             illnesses, and their contribution to mechanism of treatment
             response. © 2008 Nature Publishing Group All rights
             reserved.},
   Language = {eng},
   Doi = {10.1038/npp.2008.52},
   Key = {Bigos2008}
}

@article{Gianaros2008a,
   Author = {Gianaros, PJ and Sheu, LK and Matthews, KA and Jennings, RR and Manuck,
             SB and Hariri, AR},
   Title = {Individual differences in stressor-evoked blood pressure
             reactivity vary with activation, volume, and functional
             connectivity of the amygdala},
   Journal = {The Journal of neuroscience : the official journal of the
             Society for Neuroscience},
   Volume = {28},
   Number = {4},
   Pages = {990-999},
   Address = {Department of Psychiatry, University of Pittsburgh,
             Pittsburgh, Pennsylvania 15213, USA. gianarospj@upmc.edu},
   Year = {2008},
   ISSN = {0270-6474},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/18216206},
   Keywords = {Adolescent • Adult • Amygdala/anatomy \&
             histology/*physiology • Blood Pressure/*physiology
             • Female • Humans • *Individuality •
             Male • Nerve Net/anatomy \& histology/*physiology
             • Organ Size/physiology • Pons/anatomy \&
             histology/physiology • Stress, Psychological/*physiopathology},
   Abstract = {Individuals who exhibit exaggerated blood pressure reactions
             to psychological stressors are at risk for hypertension,
             ventricular hypertrophy, and premature atherosclerosis;
             however, the neural systems mediating exaggerated blood
             pressure reactivity and associated cardiovascular risk in
             humans remain poorly defined. Animal models indicate that
             the amygdala orchestrates stressor-evoked blood pressure
             reactions via reciprocal signaling with corticolimbic and
             brainstem cardiovascular-regulatory circuits. Based on these
             models, we used a multimodal neuroimaging approach to
             determine whether human individual differences in
             stressor-evoked blood pressure reactivity vary with amygdala
             activation, gray matter volume, and functional connectivity
             with corticolimbic and brainstem areas implicated in
             stressor processing and cardiovascular regulation. We
             monitored mean arterial pressure (MAP) and concurrent
             functional magnetic resonance imaging BOLD signal changes in
             healthy young individuals while they completed a Stroop
             color-word stressor task, validated previously in
             epidemiological studies of cardiovascular risk. Individuals
             exhibiting greater stressor-evoked MAP reactivity showed (1)
             greater amygdala activation, (2) lower amygdala gray matter
             volume, and (3) stronger positive functional connectivity
             between the amygdala and perigenual anterior cingulate
             cortex and brainstem pons. Individual differences in
             amygdala activation, gray matter volume, and functional
             connectivity with corticolimbic and brainstem circuits may
             partly underpin cardiovascular disease risk by impacting
             stressor-evoked blood pressure reactivity. Copyright © 2008
             Society for Neuroscience.},
   Language = {eng},
   Doi = {10.1523/JNEUROSCI.3606-07.2008},
   Key = {Gianaros2008a}
}

@article{Zhou2008,
   Author = {Zhou, Z and Zhu, G and Hariri, AR and Enoch, M-A and Scott, D and Sinha, R and Virkkunen, M and Mash, DC and Lipsky, RH and Hu, X-Z and Hodgkinson, CA and Xu, K and Buzas, B and Yuan, Q and Shen, P-H and Ferrell, RE and Manuck,
             SB and Brown, SM and Hauger, RL and Stohler, CS and Zubieta, J-K and Goldman, D},
   Title = {Genetic variation in human NPY expression affects stress
             response and emotion},
   Journal = {Nature},
   Volume = {452},
   Number = {7190},
   Pages = {997-1001},
   Address = {Laboratory of Neurogenetics, NIAAA, NIH, Bethesda, Maryland
             20892, USA.},
   Year = {2008},
   ISSN = {0028-0836},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/18385673},
   Keywords = {Alleles • Anxiety/genetics • Anxiety
             Disorders/genetics • Brain/*metabolism/physiology/physiopathology
             • *Emotions • European Continental Ancestry
             Group/genetics • Facial Expression •
             Finland/ethnology • Gene Expression
             Regulation/*genetics • Genetic Variation/*genetics
             • Haplotypes/genetics • Humans •
             Lymphocytes/metabolism • Magnetic Resonance Imaging
             • Male • Neuropeptide Y/blood/*genetics •
             Opioid Peptides/metabolism • Pain/genetics •
             Polymorphism, Single Nucleotide/genetics • RNA,
             Messenger/genetics/metabolism • Stress,
             Physiological/*genetics/psychology • United
             States/ethnology},
   Abstract = {Understanding inter-individual differences in stress
             response requires the explanation of genetic influences at
             multiple phenotypic levels, including complex behaviours and
             the metabolic responses of brain regions to emotional
             stimuli. Neuropeptide Y (NPY) is anxiolytic and its release
             is induced by stress. NPY is abundantly expressed in regions
             of the limbic system that are implicated in arousal and in
             the assignment of emotional valences to stimuli and
             memories. Here we show that haplotype-driven NPY expression
             predicts brain responses to emotional and stress challenges
             and also inversely correlates with trait anxiety. NPY
             haplotypes predicted levels of NPY messenger RNA in
             post-mortem brain and lymphoblasts, and levels of plasma
             NPY. Lower haplotype-driven NPY expression predicted higher
             emotion-induced activation of the amygdala, as well as
             diminished resiliency as assessed by pain/stress-induced
             activations of endogenous opioid neurotransmission in
             various brain regions. A single nucleotide polymorphism (SNP
             rs16147) located in the promoter region alters NPY
             expression in vitro and seems to account for more than half
             of the variation in expression in vivo. These convergent
             findings are consistent with the function of NPY as an
             anxiolytic peptide and help to explain inter-individual
             variation in resiliency to stress, a risk factor for many
             diseases. ©2008 Nature Publishing Group.},
   Language = {eng},
   Doi = {10.1038/nature06858},
   Key = {Zhou2008}
}

@article{fds251998,
   Author = {Rubino, V and Blasi, G and Latorre, V and Fazio, L and d'Errico, I and Mazzola, V and Caforio, G and Nardini, M and Popolizio, T and Hariri, A and Arciero, G and Bertolino, A},
   Title = {Activity in medial prefrontal cortex during cognitive
             evaluation of threatening stimuli as a function of
             personality style.},
   Journal = {Brain Research Bulletin},
   Volume = {74},
   Number = {4},
   Pages = {250-257},
   Year = {2007},
   Month = {September},
   ISSN = {0361-9230},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/17720547},
   Abstract = {Cognitive evaluation of emotional stimuli involves a network
             of brain regions including the medial prefrontal cortex
             (mPFC). However, threatening stimuli may be perceived with
             differential salience in different individuals. The goal of
             our study was to evaluate how different personality styles
             are associated with differential modulation of brain
             activity during explicit recognition of fearful and angry
             facial expressions. Twenty-eight healthy subjects underwent
             fMRI. Based on a cognitivist model, subjects were
             categorized according to how they attribute salience to
             emotional stimuli and how they regulate their emotional
             activation. We compared 14 phobic prone (PP) subjects, whose
             identity is more centered on the inner experience ("inward")
             and around control of environmental threat, and 14 eating
             disorders prone (EDP) subjects, whose identity is more
             centered on external referential contexts ("outward") and
             much less around control of threatening stimuli. During fMRI
             subjects either matched the identity of one of two angry and
             fearful faces to that of a simultaneously presented target
             face or identified the expression of a target face by
             choosing one of two simultaneously presented linguistic
             labels. The fMRI results indicated that PP subjects had
             greater mPFC activation when compared with EDP subjects
             during cognitive labeling of threatening stimuli. Activity
             in the mPFC also correlated with personality style scores.
             These results demonstrate that PP subjects recruit greater
             neuronal resources in mPFC whose activity is associated with
             cognitive aspects that are closely intertwined with
             emotional processing. These findings are consistent with the
             contention that cognitive evaluation and salience of
             emotional stimuli are associated with different personality
             styles.},
   Doi = {10.1016/j.brainresbull.2007.06.019},
   Key = {fds251998}
}

@article{fds251996,
   Author = {Fisher, PM and Meltzer, CC and Ziolko, SK and Price, JC and Moses-Kolko,
             EL and Berga, SL and Hariri, AR},
   Title = {Erratum: Capacity for 5-HT1A-mediated autoregulation
             predicts amygdala reactivity (Nature Neuroscience (2006) 9
             (1362-1363))},
   Journal = {Nature Neuroscience},
   Volume = {10},
   Number = {2},
   Pages = {263-},
   Year = {2007},
   ISSN = {1097-6256},
   url = {http://dx.doi.org/10.1038/nn0207-263a},
   Doi = {10.1038/nn0207-263a},
   Key = {fds251996}
}

@article{fds251997,
   Author = {Hariri, AR and Fisher, PM},
   Title = {Regulation of corticolimbic reactivity via the
             5-HT1A autoreceptor in the pathophysiology and
             treatment of depression},
   Journal = {Future neurology},
   Volume = {2},
   Number = {2},
   Pages = {121-124},
   Year = {2007},
   ISSN = {1479-6708},
   url = {http://dx.doi.org/10.2217/14796708.2.2.121},
   Doi = {10.2217/14796708.2.2.121},
   Key = {fds251997}
}

@article{Manuck2007,
   Author = {Manuck, SB and Brown, SM and Forbes, EE and Hariri,
             AR},
   Title = {Temporal stability of individual differences in amygdala
             reactivity [6]},
   Journal = {American Journal of Psychiatry},
   Volume = {164},
   Number = {10},
   Pages = {1613-1614},
   Year = {2007},
   ISSN = {0002-953X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/17898358},
   Keywords = {Adult • Amygdala/*physiology • Anger/physiology
             • Emotions/*physiology • Fear/physiology •
             Female • Humans • *Individuality • Magnetic
             Resonance Imaging/*statistics \& numerical data • Male
             • Middle Aged • Mood Disorders/diagnosis},
   Language = {eng},
   Doi = {10.1176/appi.ajp.2007.07040609},
   Key = {Manuck2007}
}

@article{Bigos2007,
   Author = {Bigos, KL and Hariri, AR},
   Title = {Neuroimaging: Technologies at the Interface of Genes, Brain,
             and Behavior},
   Journal = {Neuroimaging Clinics of North America},
   Volume = {17},
   Number = {4},
   Pages = {459-467},
   Address = {Department of Pharmaceutical Sciences, University of
             Pittsburgh School of Pharmacy, Pittsburgh, PA 15213,
             USA.},
   Year = {2007},
   ISSN = {1052-5149},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/17983963},
   Keywords = {Behavior/*physiology • Brain/*physiology • *Brain
             Mapping • *Gene Expression • Humans •
             *Polymorphism, Genetic},
   Abstract = {Neuroimaging technologies provide a powerful approach to
             exploring the genetic basis of individual differences in
             complex behaviors and vulnerability to neuropsychiatric
             illness. Functional MRI studies have established important
             physiologic links between genetic polymorphisms and robust
             differences in information processing within distinct brain
             regions and circuits that have been linked to the
             manifestation of various disease. Neuroimaging technologies
             represent a critical tool in efforts to understand the
             neurobiology of normal and pathologic behavioral states.
             Research capitalizing on neuroimagingbased integration will
             contribute to the identification of predictive markers and
             biologic pathways for neuropsychiatric disease vulnerability
             and the generation of novel targets for therapeutic
             intervention. © 2007 Elsevier Inc. All rights
             reserved.},
   Language = {eng},
   Doi = {10.1016/j.nic.2007.09.005},
   Key = {Bigos2007}
}

@article{Conklin2007,
   Author = {Conklin, SM and Gianaros, PJ and Brown, SM and Yao, JK and Hariri, AR and Manuck, SB and Muldoon, MF},
   Title = {Long-chain omega-3 fatty acid intake is associated
             positively with corticolimbic gray matter volume in healthy
             adults},
   Journal = {Neuroscience Letters},
   Volume = {421},
   Number = {3},
   Pages = {209-212},
   Address = {Department of Psychiatry, University of Pittsburgh, School
             of Medicine, Pittsburgh, PA 15260, United States.
             conklinSM@UPMC.Edu},
   Year = {2007},
   ISSN = {0304-3940},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/17574755},
   Keywords = {Adult • Brain Mapping • Cerebral Cortex/anatomy \&
             histology/*drug effects • Fatty Acids,
             Omega-3/*administration \& dosage • Female •
             Humans • Limbic System/*anatomy \& histology/*drug
             effects • Magnetic Resonance Imaging/methods •
             Male • Middle Aged},
   Abstract = {Background: In animals, dendritic arborization and levels of
             brain derived neurotrophic factor are positively associated
             with intake of the omega-3 fatty acids. Here, we test
             whether omega-3 fatty acid intake in humans varies with
             individual differences in gray matter volume, an in vivo,
             systems-level index of neuronal integrity. Methods:
             Fifty-five healthy adults completed two 24 h dietary recall
             interviews. Intake of long-chain omega-3 fatty acids was
             categorized by tertiles. Regional gray matter volumes in a
             putative emotional brain circuitry comprised of the anterior
             cingulate cortex (ACC), amygdala and hippocampus were
             calculated using optimized voxel-based morphometry on
             high-resolution structural magnetic resonance images.
             Results: Region of interest analyses revealed positive
             associations between reported dietary omega-3 intake and
             gray matter volume in the subgenual ACC, the right
             hippocampus and the right amygdala, adjusted for total gray
             matter volume of brain. Unconstrained whole-brain analyses
             confirmed that higher intake of omega-3 fatty acids was
             selectively associated with increased greater gray matter
             volume in these and not other regions. Conclusions: Higher
             reported consumption of the long-chain omega-3 fatty acids
             is associated with greater gray matter volume in nodes of a
             corticolimbic circuitry supporting emotional arousal and
             regulation. Such associations may mediate previously
             observed effects of omega-3 fatty acids on memory, mood and
             affect regulation. © 2007 Elsevier Ireland Ltd. All rights
             reserved.},
   Language = {eng},
   Doi = {10.1016/j.neulet.2007.04.086},
   Key = {Conklin2007}
}

@article{Gianaros2007,
   Author = {Gianaros, PJ and Horenstein, JA and Cohen, S and Matthews, KA and Brown,
             SM and Flory, JD and Critchley, HD and Manuck, SB and Hariri,
             AR},
   Title = {Perigenual anterior cingulate morphology covaries with
             perceived social standing},
   Journal = {Social Cognitive and Affective Neuroscience},
   Volume = {2},
   Number = {3},
   Pages = {161-173},
   Address = {Department of Psychiatry, University of Pittsburgh,
             Pittsburgh, PA 15213, USA. gianarospj@upmc.edu},
   Year = {2007},
   ISSN = {1749-5016},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/18418472},
   Keywords = {Adult • Cognition/physiology • Female • Gyrus
             Cinguli/*anatomy \& histology/physiology • Humans
             • Male • Middle Aged • *Social Class •
             *Social Perception},
   Abstract = {Low socioeconomic status (SES) increases the risk for
             developing psychiatric and chronic medical disorders. A
             stress-related pathway by which low SES may affect mental
             and physical health is through the perception of holding a
             low social standing, termed low subjective social status.
             This proposal implicates overlapping brain regions mediating
             stress reactivity and socioemotional behaviors as
             neuroanatomical substrates that could plausibly link
             subjective social status to health-related outcomes. In a
             test of this proposal, we used a computational structural
             neuroimaging method (voxel-based morphometry) in a healthy
             community sample to examine the relationships between
             reports of subjective social status and regional gray matter
             volume. Results showed that after accounting for potential
             demographic confounds, subclinical depressive symptoms,
             dispositional forms of negative emotionality and
             conventional indicators of SES, self-reports of low
             subjective social status uniquely covaried with reduced gray
             matter volume in the perigenual area of the anterior
             cingulate cortex (pACC)-a brain region involved in
             experiencing emotions and regulating behavioral and
             physiological reactivity to psychosocial stress. The pACC
             may represent a neuroanatomical substrate by which perceived
             social standing relates to mental and physical health. ©
             2007 The Author(s).},
   Language = {eng},
   Doi = {10.1093/scan/nsm013},
   Key = {Gianaros2007}
}

@article{Heinz2007,
   Author = {Heinz, A and Smolka, MN and Braus, DF and Wrase, J and Beck, A and Flor, H and Mann, K and Schumann, G and Büchel, C and Hariri, AR and Weinberger,
             DR},
   Title = {Serotonin Transporter Genotype (5-HTTLPR): Effects of
             Neutral and Undefined Conditions on Amygdala
             Activation},
   Journal = {Biological Psychiatry},
   Volume = {61},
   Number = {8},
   Pages = {1011-1014},
   Address = {Department of Psychiatry, Charite University Medicine
             Berlin, Campus Charite Mitte, Germany.},
   Year = {2007},
   ISSN = {0006-3223},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/17157270},
   Keywords = {Adult • Amygdala/blood supply/*physiology •
             Emotions/*physiology • Functional Laterality •
             Gene Frequency • Genotype • Humans • Image
             Processing, Computer-Assisted/methods • Magnetic
             Resonance Imaging/methods • Male • Middle Aged
             • Oxygen/blood • Photic Stimulation •
             Polymorphism, Genetic • Serotonin Plasma Membrane
             Transport Proteins/*genetics},
   Abstract = {Background: A polymorphism of the human serotonin
             transporter gene (SCL6A4) has been associated with serotonin
             transporter expression and with processing of aversive
             stimuli in the amygdala. Functional imaging studies show
             that during the presentation of aversive versus neutral
             cues, healthy carriers of the short (s) allele showed
             stronger amygdala activation than long (l) carriers.
             However, a recent report suggested that this interaction is
             driven by amygdala deactivation during presentation of
             neutral stimuli in s carriers. Methods: Functional MRI was
             used to assess amygdala activation during the presentation
             of a fixation cross or affectively aversive or neutral
             visual stimuli in 29 healthy men. Results: Amygdala
             activation was increased in s carriers during undefined
             states such as the presentation of a fixation cross compared
             with emotionally neutral conditions. Conclusions: This
             finding suggests that s carriers show stronger amygdala
             reactivity to stimuli and contexts that are relatively
             uncertain, which we propose are stressful. © 2007 Society
             of Biological Psychiatry.},
   Language = {eng},
   Doi = {10.1016/j.biopsych.2006.08.019},
   Key = {Heinz2007}
}

@article{Lerner2007,
   Author = {Lerner, JS and Dahl, RE and Hariri, AR and Taylor,
             SE},
   Title = {Facial Expressions of Emotion Reveal Neuroendocrine and
             Cardiovascular Stress Responses},
   Journal = {Biological Psychiatry},
   Volume = {61},
   Number = {2},
   Pages = {253-260},
   Address = {Department of Social \& Decision Sciences, Carnegie Mellon
             University, Pittsburgh, PA 15213, USA. jlerner@cmu.edu},
   Year = {2007},
   ISSN = {0006-3223},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/17150197},
   Keywords = {Adolescent • Adult • Anger/physiology •
             Arousal/*physiology • Blood Pressure/*physiology •
             Emotions/*physiology • *Facial Expression • Facial
             Muscles/physiology • Fear/physiology • Female
             • Heart Rate/*physiology • Humans •
             Hydrocortisone/*blood • Hypothalamo-Hypophyseal
             System/*physiology • Male • Pituitary-Adrenal
             System/*physiology • Principal Component Analysis
             • Problem Solving/physiology • Stress,
             Psychological/complications},
   Abstract = {Background: The classic conception of stress involves
             undifferentiated negative affect and corresponding
             biological reactivity. The present study hypothesized a new
             conception, disaggregating stress into emotion-specific,
             contrasting patterns of biological response. Specifically,
             it hypothesized contrasting patterns for indignation
             (comprised of anger and disgust) versus fear. Moreover, it
             hypothesized that facial expressions of these emotions would
             signal corresponding biological stress responses. Methods:
             Ninety-two adults engaged in annoyingly difficult
             stress-challenge tasks, during which cardiovascular
             responses, hypothalamic-pituitary-adrenocortical (HPA) axis
             responses (i.e., cortisol), emotional expressions (i.e.,
             facial muscle movements), and subjective emotional
             experience were assessed. Results: Pronounced individual
             differences emerged in specific emotional responses to the
             stressors. Analyses of facial expressions revealed that the
             more fear individuals displayed in response to the
             stressors, the higher their cardiovascular and cortisol
             responses to stress. By contrast, the more indignation
             individuals displayed in response to the same stressors the
             lower their cortisol levels and cardiovascular responses.
             Conclusions: Facial expressions of emotion signal biological
             responses to stress. Fear expressions signal elevated
             cortisol and cardiovascular reactivity; indignation signals
             attenuated cortisol and cardiovascular reactivity, patterns
             that implicate individual differences in stress appraisals.
             Rather than conceptualizing stress as generalized negative
             affect, studies can be informed by this emotion-specific
             approach to stress responses. © 2007 Society of Biological
             Psychiatry.},
   Language = {eng},
   Doi = {10.1016/j.biopsych.2006.08.016},
   Key = {Lerner2007}
}

@article{fds251995,
   Author = {Bertolino, A and Rubino, V and Sambataro, F and Blasi, G and Latorre, V and Fazio, L and Caforio, G and Petruzzella, V and Kolachana, B and Hariri,
             A and Meyer-Lindenberg, A and Nardini, M and Weinberger, DR and Scarabino, T},
   Title = {Prefrontal-hippocampal coupling during memory processing is
             modulated by COMT val158met genotype.},
   Journal = {Biological Psychiatry},
   Volume = {60},
   Number = {11},
   Pages = {1250-1258},
   Year = {2006},
   Month = {December},
   ISSN = {0006-3223},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/16950222},
   Abstract = {BACKGROUND: Studies in humans and in animals have
             demonstrated that a network of brain regions is involved in
             performance of declarative and recognition memory tasks.
             This network includes the hippocampal formation (HF) as well
             as the ventrolateral prefrontal cortex (VLPFC). Studies in
             animals have suggested that the relationship between these
             brain regions is strongly modulated by dopamine. METHODS:
             Using fMRI in healthy humans matched for a series of
             demographic and genetic variables, we studied the effect of
             the COMT val158met polymorphism on function of HF and VLPFC
             as well as on their functional coupling during recognition
             memory. RESULTS: The COMT Val allele was associated with:
             relatively poorer performance at retrieval; reduced
             recruitment of neuronal resources in HF and increased
             recruitment in VLPFC during both encoding and retrieval; and
             unfavorable functional coupling between these two regions at
             retrieval. Moreover, functional coupling during retrieval
             was predictive of behavioral accuracy. CONCLUSIONS: These
             results shed new light on individual differences in
             responsivity and connectivity between HF and VLPFC related
             to genetic modulation of dopamine, a mechanism accounting at
             least in part for individual differences in recognition
             memory performance.},
   Doi = {10.1016/j.biopsych.2006.03.078},
   Key = {fds251995}
}

@article{fds251994,
   Author = {Goldberg, TE and Straub, RE and Callicott, JH and Hariri, A and Mattay,
             VS and Bigelow, L and Coppola, R and Egan, MF and Weinberger,
             DR},
   Title = {The G72/G30 gene complex and cognitive abnormalities in
             schizophrenia.},
   Journal = {Neuropsychopharmacology (Nature)},
   Volume = {31},
   Number = {9},
   Pages = {2022-2032},
   Year = {2006},
   Month = {September},
   ISSN = {0893-133X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/16554747},
   Abstract = {A recently discovered gene complex, G72/G30 (hereafter G72,
             but now termed DAOA), was found to be associated with
             schizophrenia and with bipolar disorder, possibly because of
             an indirect effect on NMDA neurotransmission. In principle,
             if G72 increases risk for psychosis by this mechanism, it
             might impact with greater penetrance those cortically based
             cognitive and neurophysiological functions associated with
             NMDA signaling. We performed two independent family-based
             association studies (one sample contained more than 200
             families and the other more than 65) of multiple SNPs in the
             G72 region and of multiple SNPs in the gene for D-amino acid
             oxidase (DAAO), which may be modulated by G72. We examined
             the relationship between select cognitive measures in
             attention, working memory, and episodic memory and a
             restricted set of G72 SNPs in over 600 normal controls,
             schizophrenic patients, and their nonpsychotic siblings
             using mixed model ANOVAs. We also determined genotype
             effects on neurophysiology measures in normal controls using
             the fMRI BOLD response obtained during activation procedures
             involving either episodic memory or working memory. There
             were no significant single G72 SNP associations and clinical
             diagnosis in either sample, though one approached
             significance (p=0.06). Diagnosis by genotype interaction
             effects for G72 SNP 10 were significant for cognitive
             variables assessing working memory and attention (p=0.05),
             and at the trend level for episodic memory, such that in the
             schizophrenia group an exaggerated allele load effect in the
             predicted directions was observed. In the fMRI paradigms, a
             strong effect of G72 SNP 10 genotype was observed on BOLD
             activation in the hippocampus during the episodic memory
             paradigm. Tests of association with DAAO were consistently
             nonsignificant. We present evidence that SNP variations in
             the G72 gene region increase risk of cognitive impairment in
             schizophrenia. SNP variations were not strongly associated
             with clinical diagnosis in family-based analyses.},
   Doi = {10.1038/sj.npp.1301049},
   Key = {fds251994}
}

@article{Drabant2006,
   Author = {Drabant, E. M. and Hariri, A. R. and Meyer-Lindenberg, A. and Munoz, K. E. and Mattay, V. S. and Kolachana, B. S. and Egan, M. F. and Weinberger, D. R.},
   Title = {Catechol O-methyltransferase val158met genotype and neural
             mechanisms related to affective arousal and
             regulation},
   Journal = {Archives of general psychiatry},
   Volume = {63},
   Number = {12},
   Pages = {1396--406},
   Address = {Genes, Cognition, and Psychosis Program, Intramural Research
             Program, National Institute of Mental Health, National
             Institutes of Health/DHHS, 10 Center Drive, Bethesda, MD
             20892, USA.},
   Year = {2006},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/17146014},
   Keywords = {Adult • Affect/*physiology/*radiation effects •
             Affective Symptoms/diagnosis/*genetics •
             Amygdala/physiology • Arousal/genetics/*physiology
             • Brain Mapping/methods • Catechol
             O-Methyltransferase/*genetics • Exploratory
             Behavior/physiology • Facial Expression • Female
             • Genotype • Humans • Limbic
             System/*physiology • Magnetic Resonance
             Imaging/statistics \& numerical data • Male •
             Methionine/genetics • Neural Pathways/physiology •
             Oxygen/blood • Polymorphism, Genetic/*physiology •
             Prefrontal Cortex/*physiology • Synaptic
             Transmission/physiology • Temperament/physiology •
             Valine/genetics • Visual Perception/physiology},
   Abstract = {CONTEXT: Catechol O-methyltransferase (COMT), the major
             enzyme determining cortical dopamine flux, has a common
             functional polymorphism (val(158)met) that affects
             prefrontal function and working memory capacity and has also
             been associated with anxiety and emotional dysregulation.
             OBJECTIVES: To examine COMT val(158)met effects on
             corticolimbic circuitry reactivity and functional
             connectivity during processing of biologically salient
             stimuli, as well as the relationship to the temperamental
             trait of novelty seeking. DESIGN: Within-subject functional
             magnetic resonance imaging study. SETTING: National
             Institute of Mental Health, Genes, Cognition, and Psychosis
             Program, Bethesda, Md. Patients One hundred one healthy
             subjects of both sexes. RESULTS: We found that the met
             allele was associated with a dose-dependent increase in
             hippocampal formation and ventrolateral prefrontal cortex
             activation during viewing of faces displaying negative
             emotion. In met/met homozygotes, limbic and prefrontal
             regions showed increased functional coupling. Moreover, in
             these same subjects, the magnitude of amygdala-orbitofrontal
             coupling was inversely correlated with novelty seeking, an
             index of temperamental inflexibility. CONCLUSIONS: Our
             results indicate that heritable variation in dopamine
             neurotransmission associated with the met allele of the COMT
             polymorphism results in heightened reactivity and
             connectivity in corticolimbic circuits. This may reflect a
             genetic predisposition for inflexible processing of
             affective stimuli, a mechanism possibly accounting for
             aspects of arousal and behavioral control that contribute to
             emotional dysregulation previously reported in met/met
             individuals.},
   Language = {eng},
   Doi = {10.1001/archpsyc.63.12.1396},
   Key = {Drabant2006}
}

@article{Fisher2006,
   Author = {Fisher, P. M. and Meltzer, C. C. and Ziolko, S. K. and Price, J. C. and Moses-Kolko, E. L. and Berga, S. L. and Hariri, A. R.},
   Title = {Capacity for 5-HT1A-mediated autoregulation predicts
             amygdala reactivity},
   Journal = {Nature neuroscience},
   Volume = {9},
   Number = {11},
   Pages = {1362--3},
   Address = {Department of Psychiatry, University of Pittsburgh School of
             Medicine, Pittsburgh, Pennsylvania 15213,
             USA.},
   Year = {2006},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/17013380},
   Keywords = {Adult • Amygdala/*physiology •
             Depression/metabolism • Feedback/physiology •
             Homeostasis/*physiology • Humans • Magnetic
             Resonance Imaging • Oxygen/blood •
             Piperazines/pharmacology • Positron-Emission Tomography
             • Pyridines/pharmacology • Receptor, Serotonin,
             5-HT1A/drug effects/*physiology • Serotonin
             Antagonists/pharmacology},
   Abstract = {We examined the contribution of 5-HT1A autoreceptors (with
             [11C]WAY100635 positron emission tomography) to amygdala
             reactivity (with blood oxygenation level-dependent
             functional magnetic resonance imaging) in 20 healthy adult
             volunteers. We found a significant inverse relationship
             wherein 5-HT1A autoreceptor density predicted a notable
             30-44\% of the variability in amygdala reactivity. Our data
             suggest a potential molecular mechanism by which a reduced
             capacity for negative feedback regulation of 5-HT release is
             associated with increased amygdala reactivity.},
   Language = {eng},
   Doi = {10.1038/nn1780},
   Key = {Fisher2006}
}

@article{fds251993,
   Author = {Meyer-Lindenberg, A and Buckholtz, JW and Kolachana, B and Hariri,
             AR and Pezawas, L and Blasi, G and Wabnitz, A and Honea, R and Verchinski,
             B and Callicott, JH and Egan, M and Mattay, V and Weinberger,
             DR},
   Title = {Neural mechanisms of genetic risk for impulsivity and
             violence in humans},
   Journal = {Proceedings of the National Academy of Sciences of
             USA},
   Volume = {103},
   Number = {16},
   Pages = {6269-6274},
   Year = {2006},
   ISSN = {0027-8424},
   url = {http://dx.doi.org/10.1073/pnas.0511311103},
   Abstract = {Neurobiological factors contributing to violence in humans
             remain poorly understood. One approach to this question is
             examining allelic variation in the X-linked monoamine
             oxidase A (MAOA) gene, previously associated with impulsive
             aggression in animals and humans. Here, we have studied the
             impact of a common functional polymorphism in MAOA on brain
             structure and function assessed with MRI in a large sample
             of healthy human volunteers. We show that the low expression
             variant, associated with increased risk of violent behavior,
             predicted pronounced limbic volume reductions and
             hyperresponsive amygdala during emotional arousal, with
             diminished reactivity of regulatory prefrontal regions,
             compared with the high expression allele. In men, the low
             expression allele is also associated with changes in
             orbitofrontal volume, amygdala and hippocampus
             hyperreactivity during aversive recall, and impaired
             cingulate activation during cognitive inhibition. Our data
             identify differences in limbic circuitry for emotion
             regulation and cognitive control that may be involved in the
             association of MAOA with impulsive aggression, suggest
             neural systems-level effects of X-inactivation in human
             brain, and point toward potential targets for a biological
             approach toward violence.},
   Doi = {10.1073/pnas.0511311103},
   Key = {fds251993}
}

@article{Neumann2006,
   Author = {Neumann, SA and Brown, SM and Ferrell, RE and Flory, JD and Manuck, SB and Hariri, AR},
   Title = {Human Choline Transporter Gene Variation Is Associated with
             Corticolimbic Reactivity and Autonomic-Cholinergic
             Function},
   Journal = {Biological Psychiatry},
   Volume = {60},
   Number = {10},
   Pages = {1155-1162},
   Address = {Department of Psychiatry and Behavioral Sciences, Eastern
             Virginia Medical School, 825 Fairfax Avenue, Norfolk, VA
             23501. Neumans@evms.edu},
   Year = {2006},
   ISSN = {0006-3223},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/16876130},
   Keywords = {Adult • Autonomic Nervous System/*physiology •
             Brain Mapping • Cerebral Cortex/blood
             supply/*physiology • Choice Behavior/physiology •
             Electrocardiography • European Continental Ancestry
             Group • Female • *Genetic Variation • Heart
             Rate/physiology • Humans • Image Processing,
             Computer-Assisted/methods • Limbic System/blood
             supply/*physiology • Magnetic Resonance Imaging/methods
             • Male • Membrane Transport Proteins/*genetics
             • Middle Aged • Neural Pathways/blood
             supply/*physiology • Neuropsychological Tests •
             Oxygen/blood • Polymorphism, Single
             Nucleotide},
   Abstract = {Background: Our previous work has shown genetic variation in
             the human choline transporter gene (CHT1) to be associated
             with depressive symptoms and autonomic cardiac (cholinergic)
             dysregulation. Here, functional magnetic resonance imaging
             (fMRI) was used to examine the relation between a single
             nucleotide polymorphism (SNP) in CHT1 on regional brain
             reactivity relevant to autonomic (cholinergic) function.
             Methods: Thirty-two participants of European ancestry (18
             men, 14 women; age: 33-54 years) completed an fMRI protocol
             using corticolimbic reactivity and prefrontal inhibitory
             control paradigms. Resting cholinergic function, as measured
             by heart rate variability (HRV), was quantified from
             electrocardiogram Subjects were genotyped for a CHT1 G/T
             SNP. Results: GG homozygotes had greater right (R) dorsal
             amygdala (p &lt; .008), bilateral anterior cingulate (p &lt;
             .009), and R caudate reactivity (p &lt; .015) than T-allele
             carriers. Heart rate variability was related to R frontal
             cortex (Brodmann Areas 6, 9, and 46), R hippocampal
             formation, bilateral caudate, and bilateral anterior
             cingulate reactivity (p's &lt; .007). Conclusions: CHT1
             variation is related to differences in a distributed
             corticolimbic circuitry mediating behavioral and physiologic
             arousal. These relations may contribute to a biological
             mechanism by which genetic variation in cholinergic
             neurotransmission affects cognition, mood, and autonomic
             cardiac function. © 2006 Society of Biological
             Psychiatry.},
   Language = {eng},
   Doi = {10.1016/j.biopsych.2006.03.059},
   Key = {Neumann2006}
}

@article{Brown2006b,
   Author = {Brown, SM and Hariri, AR},
   Title = {Neuroimaging studies of serotonin gene polymorphisms:
             Exploring the interplay of genes, brain, and
             behavior},
   Journal = {Cognitive, Affective, & Behaviorial Neuroscience},
   Volume = {6},
   Number = {1},
   Pages = {44-52},
   Address = {Department of Psychiatry, University of Pittsburgh School of
             Medicine, Western Psychiatric Institute and Clinic, 3811
             O'Hara Street, Room E-729, Pittsburgh, PA 15213-2593,
             USA.},
   Year = {2006},
   ISSN = {1530-7026},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/16869228},
   Keywords = {Animals • Behavior/*physiology • Brain/*anatomy \&
             histology/*physiology • Brain Mapping • Diagnostic
             Imaging/methods • Emotions/physiology • Humans
             • Nerve Net • *Polymorphism, Genetic •
             Serotonin/*genetics},
   Abstract = {Because of the unique ability it provides to investigate
             information processing at the level of neural systems,
             functional neuroimaging is a powerful tool to explore the
             relationship between genes, brain, and behavior. Recently,
             functional neuroimaging has provided dramatic illustrations
             of how a promoter polymorphism in the human serotonin
             transporter gene, which has been weakly related to several
             dimensions of emotional behaviors (such as neuroticism and
             anxiety traits), is strongly related to the engagement of
             neural systems-namely, the amygdala and subgenual prefrontal
             cortex, subserving emotional information processing. This
             review will outline the experimental strategy by which these
             genetic effects on brain function have been explored and
             highlight the effectiveness of this strategy to delineate
             biological pathways and mechanisms contributing to the
             emergence of individual differences in brain function that
             potentially bias behavior and risk for psychiatric illness.
             Copyright 2006 Psychonomic Society, Inc.},
   Language = {eng},
   Doi = {10.3758/CABN.6.1.44},
   Key = {Brown2006b}
}

@article{Viding2006,
   Author = {Viding, E and Williamson, DE and Hariri, AR},
   Title = {Developmental imaging genetics: Challenges and promises for
             translational research},
   Journal = {Development and Psychopathology},
   Volume = {18},
   Number = {3},
   Pages = {877-892},
   Address = {University College London.},
   Year = {2006},
   ISSN = {0954-5794},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/17152405},
   Keywords = {Antisocial Personality Disorder/genetics/pathology/physiopathology
             • Brain/*pathology/*physiopathology •
             *Electroencephalography • Humans •
             *Interdisciplinary Communication • *Magnetic Resonance
             Imaging • *Mental Disorders/genetics/pathology/physiopathology
             • Research/*standards • Serotonin/genetics},
   Abstract = {Advances in molecular biology, neuroimaging, genetic
             epidemiology, and developmental psychopathology have
             provided a unique opportunity to explore the interplay of
             genes, brain, and behavior within a translational research
             framework. Herein, we begin by outlining an experimental
             strategy by which genetic effects on brain function can be
             explored using neuroimaging, namely, imaging genetics. We
             next describe some major findings in imaging genetics to
             highlight the effectiveness of this strategy for delineating
             biological pathways and mechanisms by which individual
             differences in brain function emerge and potentially bias
             behavior and risk for psychiatric illness. We then discuss
             the importance of applying imaging genetics to the study of
             psychopathology within a developmental framework. By
             beginning to move toward a systems-level approach to
             understanding pathways to behavioral outcomes as they are
             expressed across development, it is anticipated that we will
             move closer to understanding the complexities of the
             specific mechanisms involved in the etiology of psychiatric
             disease. Despite the numerous challenges that lie ahead, we
             believe that developmental imaging genetics has potential to
             yield highly informative results that will ultimately
             translate into public health benefits. We attempt to set out
             guidelines and provide exemplars that may help in designing
             fruitful translational research applications that
             incorporate a developmental imaging genetics strategy. ©
             2006 Cambridge University Press.},
   Language = {eng},
   Doi = {10.1017/S0954579406060433},
   Key = {Viding2006}
}

@article{Hariri2006a,
   Author = {Hariri, AR and Lewis, DA},
   Title = {Genetics and the future of clinical psychiatry},
   Journal = {American Journal of Psychiatry},
   Volume = {163},
   Number = {10},
   Pages = {1676-1678},
   Year = {2006},
   ISSN = {0002-953X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/17012672},
   Keywords = {Forecasting • Genetics, Medical • Mental
             Disorders/genetics • Psychiatry/*trends},
   Language = {eng},
   Doi = {10.1176/appi.ajp.163.10.1676},
   Key = {Hariri2006a}
}

@article{Hariri2006e,
   Author = {Tamminga, CA and Hariri, AR and Brown, SM},
   Title = {Serotonin},
   Journal = {American Journal of Psychiatry},
   Volume = {163},
   Number = {1},
   Pages = {12-},
   Year = {2006},
   ISSN = {0002-953X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/16390882},
   Keywords = {Amygdala/*metabolism/physiopathology • European
             Continental Ancestry Group/genetics • Gene Frequency
             • Genetic Variation • Genotype • Humans
             • Mood Disorders/*genetics/physiopathology •
             Serotonin/genetics/metabolism/*physiology • Serotonin
             Plasma Membrane Transport Proteins/*genetics/physiology},
   Language = {eng},
   Doi = {10.1176/appi.ajp.163.1.12},
   Key = {Hariri2006e}
}

@article{Hariri2006b,
   Author = {Hariri, AR and Holmes, A},
   Title = {Genetics of emotional regulation: the role of the serotonin
             transporter in neural function},
   Journal = {Trends in Cognitive Sciences},
   Volume = {10},
   Number = {4},
   Pages = {182-191},
   Address = {Department of Psychiatry and Center for the Neural Basis of
             Cognition, University of Pittsburgh, Pittsburgh,
             Pennsylvania 15213, USA. haririar@upmc.edu},
   Year = {2006},
   ISSN = {1364-6613},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/16530463},
   Keywords = {Amygdala/pathology/physiology • Animals •
             Emotions/*physiology • *Genetic Variation • Humans
             • Models, Neurological • Mood Disorders/classification/*genetics
             • Serotonin Plasma Membrane Transport
             Proteins/*genetics/metabolism},
   Abstract = {Identifying biological mechanisms through which genes lead
             to individual differences in emotional behavior is paramount
             to our understanding of how such differences confer risk for
             neuropsychiatric illness. The emergence of techniques such
             as in vivo imaging of brain function in humans and genetic
             engineering in rodents has provided important new insights
             into the impact of serotonin (5-HT), a key modulator of
             emotional behavior, on neural systems subserving anxiety and
             depression. A major finding has been the discovery of
             genetic variation in a crucial regulatory molecule within
             the 5-HT system, the 5HT transporter (5-HTT), and its
             influence on emotional traits. The study of the 5-HTT
             provides a new foundation for understanding the
             neurobiological and genetic basis of emotional regulation
             and affective illness.},
   Language = {eng},
   Doi = {10.1016/j.tics.2006.02.011},
   Key = {Hariri2006b}
}

@article{Hariri2006c,
   Author = {Hariri, AR and Drabant, EM and Weinberger, DR},
   Title = {Imaging Genetics: Perspectives from Studies of Genetically
             Driven Variation in Serotonin Function and Corticolimbic
             Affective Processing},
   Journal = {Biological Psychiatry},
   Volume = {59},
   Number = {10},
   Pages = {888-897},
   Address = {Department of Psychiatry, University of Pittsburgh School of
             Medicine, Pittsburgh, Pennsylvania 15213-2593,
             USA.},
   Year = {2006},
   ISSN = {0006-3223},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/16442081},
   Keywords = {Alleles • Amygdala/*physiopathology • *Diagnostic
             Imaging • Emotions/*physiology • Genetic
             Variation/*genetics • Humans • Mood
             Disorders/*genetics/physiopathology • Neural
             Pathways/physiopathology • Polymorphism,
             Genetic/*genetics • Prefrontal Cortex/*physiopathology
             • Serotonin/*genetics/physiology • Serotonin
             Plasma Membrane Transport Proteins/genetics • Synaptic
             Transmission/*genetics},
   Abstract = {Advances in molecular biology and neuroimaging have provided
             a unique opportunity to explore the relationships between
             genes, brain, and behavior. In this review, we will briefly
             outline the rationale for studying genetic effects on brain
             function with neuroimaging. We will then use studies of
             genetically driven variation in serotonin transporter
             function on corticolimbic structure and function to
             highlight the effectiveness of this strategy to delineate
             biological pathways and mechanisms by which individual
             differences in brain function emerge and potentially bias
             behavior and risk for psychiatric illness. In a series of
             studies, a relatively frequent regulatory variant of the
             human serotonin transporter gene (5-HTTLPR) has been
             demonstrated to bias the reactivity of the amygdala to
             salient environmental cues. Moreover, the 5-HTTLPR affects
             the development of a broader corticolimbic circuit and
             alters the functional integration of emotional information
             between the amygdala and medial prefrontal cortex. In turn,
             corticolimbic circuit function predicts individual
             differences in an experimental index of temperamental
             anxiety and, thus, might reflect a predictive biological
             marker of increased risk for mood disorders associated with
             the 5-HTTLPR. © 2006 Society of Biological
             Psychiatry.},
   Language = {eng},
   Doi = {10.1016/j.biopsych.2005.11.005},
   Key = {Hariri2006c}
}

@article{fds252080,
   Author = {Drabant, EM and Hariri, AR and Meyer-Lindenberg, A and Munoz, KE and Mattay, VS and Kolachana, BS and Egan, MF and Weinberger,
             DR},
   Title = {Catechol O-methyltransferase val158met genotype
             and neural mechanisms related to affective arousal and
             regulation},
   Journal = {Archives of General Psychiatry},
   Volume = {63},
   Number = {12},
   Pages = {1396-1406},
   Year = {2006},
   ISSN = {0003-990X},
   url = {http://dx.doi.org/10.1001/archpsyc.63.12.1396},
   Abstract = {Context: Catechol O-methyltransferase (COMT), the major
             enzyme determining cortical dopamine flux, has a common
             functional polymorphism (val 158met) that affects prefrontal
             function and working memory capacity and has also been
             associated with anxiety and emotional dysregulation.
             Objectives: To examine COMT val158met effects on
             corticolimbic circuitry reactivity and functional
             connectivity during processing of biologically salient
             stimuli, as well as the relationship to the temperamental
             trait of novelty seeking. Design: Within-subject functional
             magnetic resonance imaging study. Setting: National
             Institute of Mental Health, Genes, Cognition, and Psychosis
             Program, Bethesda, Md. Patients: One hundred one healthy
             subjects of both sexes. Results: We found that the met
             allele was associated with a dose-dependent increase in
             hippocampal formation and ventrolateral prefrontal cortex
             activation during viewing of faces displaying negative
             emotion. In met/met homozygotes, limbic and prefrontal
             regions showed increased functional coupling. Moreover, in
             these same subjects, the magnitude of amygdala-orbitofrontal
             coupling was inversely correlated with novelty seeking, an
             index of temperamental inflexibility. Conclusions: Our
             results indicate that heritable variation in dopamine
             neurotransmission associated with the met allele of the COMT
             polymorphism results in heightened reactivity and
             connectivity in corticolimbic circuits. This may reflect a
             genetic predisposition for inflexible processing of
             affective stimuli, a mechanism possibly accounting for
             aspects of arousal and behavioral control that contribute to
             emotional dysregulation previously reported in met/met
             individuals. ©2006 American Medical Association. All rights
             reserved.},
   Doi = {10.1001/archpsyc.63.12.1396},
   Key = {fds252080}
}

@article{fds252081,
   Author = {Fisher, PM and Meltzer, CC and Ziolko, SK and Price, JC and Hariri,
             AR},
   Title = {Capacity for 5-HT1A-mediated autoregulation
             predicts amygdala reactivity},
   Journal = {Nature Neuroscience},
   Volume = {9},
   Number = {11},
   Pages = {1362-1363},
   Year = {2006},
   ISSN = {1097-6256},
   url = {http://dx.doi.org/10.1038/nn1780},
   Abstract = {We examined the contribution of 5-HT1A autoreceptors (with
             [11C]WAY100635 positron emission tomography) to amygdala
             reactivity (with blood oxygenation level-dependent
             functional magnetic resonance imaging) in 20 healthy adult
             volunteers. We found a significant inverse relationship
             wherein 5-HT1A autoreceptor density predicted a notable
             30-44% of the variability in amygdala reactivity. Our data
             suggest a potential molecular mechanism by which a reduced
             capacity for negative feedback regulation of 5-HT release is
             associated with increased amygdala reactivity. © 2006
             Nature Publishing Group.},
   Doi = {10.1038/nn1780},
   Key = {fds252081}
}

@article{Hariri2006d,
   Author = {Hariri, AR and Brown, SM and Williamson, DE and Flory, JD and Wit, HD and Manuck, SB},
   Title = {Preference for immediate over delayed rewards is associated
             with magnitude of ventral striatal activity},
   Journal = {The Journal of neuroscience : the official journal of the
             Society for Neuroscience},
   Volume = {26},
   Number = {51},
   Pages = {13213-13217},
   Address = {Department of Psychiatry, University of Pittsburgh,
             Pittsburgh, Pennsylvania 15213, USA. haririar@upmc.edu},
   Year = {2006},
   ISSN = {0270-6474},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/17182771},
   Keywords = {Adult • Basal Ganglia/*physiology • Behavior,
             Addictive/physiopathology/psychology • Choice
             Behavior/*physiology • Feedback, Psychological/physiology
             • Female • Humans • Impulsive
             Behavior/physiopathology/psychology • Male •
             Middle Aged • Nerve Net/physiology • *Reward
             • Risk Factors • Time Factors},
   Abstract = {Discounting future outcomes as a function of their deferred
             availability underlies much of human decision making.
             Discounting, or preference for immediate over delayed
             rewards of larger value, is often associated with
             impulsivity and is a risk factor for addictive disorders
             such as pathological gambling, cigarette smoking, and drug
             and alcohol abuse. The ventral striatum (VS) is involved in
             mediating behavioral responses and physiological states
             associated with reward, and dysregulation of the VS
             contributes to addiction, perhaps by affecting impulsive
             decision-making. Behavioral tests of delay discounting (DD),
             which index preference for smaller immediate over larger
             delayed rewards, covary with impulsive tendencies in humans.
             In the current study, we examined the relationship between
             individual differences in DD, measured in a behavioral
             assessment, and VS activity measured with blood oxygenation
             level-dependent functional magnetic resonance imaging, in 45
             adult volunteers. VS activity was determined using a task
             involving positive and negative feedback with monetary
             reward. Analyses revealed that individual differences in DD
             correlate positively with magnitude of VS activation in
             response to both positive and negative feedback, compared
             with a no-feedback control condition. Variability in DD was
             also associated with differential VS activation in response
             to positive, compared with negative, feedback. Collectively,
             our results suggest that increased preference for smaller
             immediate over larger delayed rewards reflects both a
             relatively indiscriminate and hyper-reactive VS circuitry.
             They also highlight a specific neurocognitive mechanism that
             may contribute to increased risk for addiction. Copyright ©
             2006 Society for Neuroscience.},
   Language = {eng},
   Doi = {10.1523/JNEUROSCI.3446-06.2006},
   Key = {Hariri2006d}
}

@article{Brown2006a,
   Author = {Brown, SM and Manuck, SB and Flory, JD and Hariri,
             AR},
   Title = {Neural basis of individual differences in impulsivity:
             Contributions of corticolimbic circuits for behavioral
             arousal and control},
   Journal = {Emotion},
   Volume = {6},
   Number = {2},
   Pages = {239-245},
   Address = {Department of Psychiatry, University of Pittsburgh,
             Pittsburgh, PA, USA.},
   Year = {2006},
   ISSN = {1528-3542},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/16768556},
   Keywords = {Adult • Amygdala/*physiopathology •
             Arousal/*physiology • Brain/*physiopathology •
             Cerebral Cortex/*physiopathology • Female • Humans
             • Impulse Control Disorders/diagnosis/*physiopathology
             • Limbic System/*physiopathology • Magnetic
             Resonance Imaging • Male • Middle Aged •
             Nerve Net/*physiology • Neural Inhibition/*physiology
             • Prefrontal Cortex/physiopathology • Severity of
             Illness Index • *Social Control, Informal},
   Abstract = {The objective of the current study was to analyze the neural
             correlates of behavioral arousal and inhibitory control as
             they relate to individual differences in impulsivity via
             well-established functional MRI amygdala reactivity and
             prefrontal inhibitory control paradigms in healthy adult
             subjects. Impulsivity correlated positively with activity of
             the bilateral ventral amygdala, parahippocampal gyrus,
             dorsal anterior cingulate gyrus (BA 32), and bilateral
             caudate. Conversely, impulsivity correlated negatively with
             activity of the dorsal amygdala and ventral prefrontal
             cortex (BA 47). Together, these findings suggest that
             dispositional impulsivity is influenced by the functional
             interplay of corticolimbic behavioral arousal and control
             circuits. Copyright 2006 by the American Psychological
             Association.},
   Language = {eng},
   Doi = {10.1037/1528-3542.6.2.239},
   Key = {Brown2006a}
}

@article{Mattay2006,
   Author = {Mattay, VS and Fera, F and Tessitore, A and Hariri, AR and Berman, KF and Das, S and Meyer-Lindenberg, A and Goldberg, TE and Callicott, JH and Weinberger, DR},
   Title = {Neurophysiological correlates of age-related changes in
             working memory capacity},
   Journal = {Neuroscience Letters},
   Volume = {392},
   Number = {1-2},
   Pages = {32-37},
   Address = {Clinical Brain Disorders Branch, Genes, Cognition and
             Psychosis Program, National Institute of Mental Health,
             National Institutes of Health, 9000 Rockville Pike,
             Bethesda, MD 20892, USA. vsm@mail.nih.gov},
   Year = {2006},
   ISSN = {0304-3940},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/16213083},
   Keywords = {Adult • Age Factors • Aged •
             Aging/*physiology • Drug Combinations • Female
             • Humans • Magnetic Resonance Imaging/methods
             • Male • Memory, Short-Term/*physiology •
             Middle Aged • Neuropsychological Tests/statistics \&
             numerical data • Peroxides/blood • Prefrontal
             Cortex/blood supply/*physiology • Reaction
             Time/physiology • Urea/analogs \& derivatives/blood},
   Abstract = {Cognitive abilities such as working memory (WM) capacity
             decrease with age. To determine the neurophysiological
             correlates of age-related reduction in working memory
             capacity, we studied 10 young subjects (&lt;35 years of age;
             mean age = 29) and twelve older subjects (&gt;55 years of
             age; mean age = 59) with whole brain blood oxygenation-level
             dependent (BOLD) fMRI on a 1.5 T GE MR scanner using a
             SPIRAL FLASH pulse sequence (TE = 24 ms, TR = 56 ms, FA =
             60°, voxel dimensions = 3.75 mm3). Subjects performed a
             modified version of the "n" back working memory task at
             different levels of increasing working memory load (1-Back,
             2-Back and 3-Back). Older subjects performed as well as the
             younger subjects at 1-Back (p = 0.4), but performed worse
             than the younger subjects at 2-Back (p &lt; 0.01) and 3-Back
             (p = 0.06). Older subjects had significantly longer reaction
             time (RT) than younger subjects (p &lt; 0.04) at all levels
             of task difficulty. Image analysis using SPM 99 revealed a
             similar distribution of cortical activity between younger
             and older subjects at all task levels. However, an analysis
             of variance revealed a significant group × task interaction
             in the prefrontal cortex bilaterally; within working memory
             capacity, as in 1-Back when the older subjects performed as
             well as the younger subjects, they showed greater prefrontal
             cortical (BA 9) activity bilaterally. At higher working
             memory loads, however, when they performed worse then the
             younger subjects, the older subjects showed relatively
             reduced activity in these prefrontal regions. These data
             suggest that, within capacity, compensatory mechanisms such
             as additional prefrontal cortical activity are called upon
             to maintain proficiency in task performance. As cognitive
             demand increases, however, they are pushed past a threshold
             beyond which physiological compensation cannot be made and,
             a decline in performance occurs. © 2005 Elsevier Ireland
             Ltd. All rights reserved.},
   Language = {eng},
   Doi = {10.1016/j.neulet.2005.09.025},
   Key = {Mattay2006}
}

@article{fds251992,
   Author = {Fera, F and Weickert, TW and Goldberg, TE and Tessitore, A and Hariri,
             A and Das, S and Lee, S and Zoltick, B and Meeter, M and Myers, CE and Gluck,
             MA and Weinberger, DR and Mattay, VS},
   Title = {Neural mechanisms underlying probabilistic category learning
             in normal aging.},
   Journal = {The Journal of neuroscience : the official journal of the
             Society for Neuroscience},
   Volume = {25},
   Number = {49},
   Pages = {11340-11348},
   Year = {2005},
   Month = {December},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/16339029},
   Abstract = {Probabilistic category learning engages neural circuitry
             that includes the prefrontal cortex and caudate nucleus, two
             regions that show prominent changes with normal aging.
             However, the specific contributions of these brain regions
             are uncertain, and the effects of normal aging have not been
             examined previously in probabilistic category learning. In
             the present study, using a blood oxygenation level-dependent
             functional magnetic resonance imaging block design, 18
             healthy young adults (mean age, 25.5 +/- 2.6 years) and 15
             older adults (mean age, 67.1 +/- 5.3 years) were assessed on
             the probabilistic category learning "weather prediction"
             test. Whole-brain functional images acquired using a 1.5T
             scanner (General Electric, Milwaukee, WI) with gradient
             echo, echo planar imaging (3/1 mm; repetition time, 3000 ms;
             echo time, 50 ms) were analyzed using second-level
             random-effects procedures [SPM99 (Statistical Parametric
             Mapping)]. Young and older adults displayed equivalent
             probabilistic category learning curves, used similar
             strategies, and activated analogous neural networks,
             including the prefrontal and parietal cortices and the
             caudate nucleus. However, the extent of caudate and
             prefrontal activation was less and parietal activation was
             greater in older participants. The percentage correct and
             reaction time were mainly positively correlated with caudate
             and prefrontal activation in young individuals but
             positively correlated with prefrontal and parietal cortices
             in older individuals. Differential activation within a
             circumscribed neural network in the context of equivalent
             learning suggests that some brain regions, such as the
             parietal cortices, may provide a compensatory mechanism for
             healthy older adults in the context of deficient prefrontal
             cortex and caudate nuclei responses.},
   Doi = {10.1523/JNEUROSCI.2736-05.2005},
   Key = {fds251992}
}

@article{fds251990,
   Author = {Bertolino, A and Arciero, G and Rubino, V and Latorre, V and De Candia,
             M and Mazzola, V and Blasi, G and Caforio, G and Hariri, A and Kolachana,
             B and Nardini, M and Weinberger, DR and Scarabino,
             T},
   Title = {Variation of human amygdala response during threatening
             stimuli as a function of 5'HTTLPR genotype and personality
             style.},
   Journal = {Biological Psychiatry},
   Volume = {57},
   Number = {12},
   Pages = {1517-1525},
   Year = {2005},
   Month = {June},
   ISSN = {0006-3223},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/15953488},
   Abstract = {BACKGROUND: In the brain, processing of fearful stimuli
             engages the amygdala, and the variability of its activity is
             associated with genetic factors as well as with emotional
             salience. The objective of this study was to explore the
             relevance of personality style for variability of amygdala
             response. METHODS: We studied two groups (n=14 in each
             group) of healthy subjects categorized by contrasting
             cognitive styles with which they attribute salience to
             fearful stimuli: so-called phobic prone subjects who
             exaggerate potential environmental threat versus so-called
             eating disorders prone subjects who tend to be much less
             centered around fear. The two groups underwent functional
             magnetic resonance imaging (fMRI) at 3T during performance
             of a perceptual task of threatening stimuli and they were
             also matched for the genotype of the 5' variable number
             tandem repeat (VNTR) polymorphism in the serotonin
             transporter. RESULTS: The fMRI results indicated that phobic
             prone subjects selectively recruit the amygdala to a larger
             extent than eating disorders prone subjects. Activity in the
             amygdala was also independently predicted by personality
             style and genotype of the serotonin transporter. Moreover,
             brain activity during a working memory task did not
             differentiate the two groups. CONCLUSIONS: The results of
             the present study suggest that aspects of personality style
             are rooted in biological responses of the fear circuitry
             associated with processing of environmental
             information.},
   Doi = {10.1016/j.biopsych.2005.02.031},
   Key = {fds251990}
}

@article{fds251989,
   Author = {Lieberman, MD and Hariri, A and Jarcho, JM and Eisenberger, NI and Bookheimer, SY},
   Title = {An fMRI investigation of race-related amygdala activity in
             African-American and Caucasian-American individuals.},
   Journal = {Nature Neuroscience},
   Volume = {8},
   Number = {6},
   Pages = {720-722},
   Year = {2005},
   Month = {June},
   ISSN = {1097-6256},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/15880106},
   Abstract = {Functional magnetic resonance imaging (fMRI) was used to
             examine the nature of amygdala sensitivity to race. Both
             African-American and Caucasian-American individuals showed
             greater amygdala activity to African-American targets than
             to Caucasian-American targets, suggesting that race-related
             amygdala activity may result from cultural learning rather
             than from the novelty of other races. Additionally, verbal
             encoding of African-American targets produced significantly
             less amygdala activity than perceptual encoding of
             African-American targets.},
   Doi = {10.1038/nn1465},
   Key = {fds251989}
}

@article{fds252011,
   Author = {Dahl, RE and Hariri, AR},
   Title = {Lessons from G. Stanley Hall: Connecting new research in
             biological sciences to the study of adolescent
             development},
   Journal = {Journal of Research on Adolescence},
   Volume = {15},
   Number = {4},
   Pages = {367-382},
   Year = {2005},
   ISSN = {1050-8392},
   url = {http://dx.doi.org/10.1111/j.1532-7795.2005.00102.x},
   Doi = {10.1111/j.1532-7795.2005.00102.x},
   Key = {fds252011}
}

@article{Winterer2005,
   Author = {Winterer, G and Hariri, AR and Goldman, D and Weinberger,
             DR},
   Title = {Neuroimaging and Human Genetics},
   Journal = {International review of neurobiology},
   Volume = {67},
   Pages = {325-383},
   Address = {Genes, Cognition and Psychosis Program, National Institute
             of Mental Health National Institutes of Health, Bethesda,
             Maryland 20892, USA.},
   Year = {2005},
   ISSN = {0074-7742},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/16291027},
   Keywords = {Brain/*anatomy \& histology/physiology • *Brain Mapping
             • *Diagnostic Imaging • *Genetics • Genetics,
             Medical • Humans},
   Abstract = {The past few years have seen a rapid expansion of the
             application of neuroimaging tools to the investigation of
             the genetics of brain structure and function. In this
             chapter, we will (1) highlight the most important steps
             during the historical development of this research field,
             (2) explain the major purposes of using neuroimaging in
             genetic research, (3) address methodological issues that are
             relevant with regard to the application of neuroimaging in
             genetic research, (4) give an overview of the present
             state-of-research, and (5) provide several examples of how
             neuroimaging was successfully applied. © 2005 Elsevier Inc.
             All rights reserved.},
   Language = {eng},
   Doi = {10.1016/S0074-7742(05)67010-9},
   Key = {Winterer2005}
}

@article{Tessitore2005,
   Author = {Tessitore, A and Hariri, AR and Fera, F and Smith, WG and Das, S and Weinberger, DR and Mattay, VS},
   Title = {Functional changes in the activity of brain regions
             underlying emotion processing in the elderly},
   Journal = {Psychiatry Research - Neuroimaging},
   Volume = {139},
   Number = {1},
   Pages = {9-18},
   Address = {Clinical Brain Disorders Branch, Genes, Cognition and
             Psychosis Program, National Institute of Mental Health,
             National Institutes of Health, 10 Center Drive, Bldg. 10,
             Room 3C108, Bethesda, MD 20892-1384, USA.},
   Year = {2005},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/15936178},
   Keywords = {Adult • *Affect • Aged • Aged, 80 and over
             • Aging/physiology • Amygdala/anatomy \& histology
             • Brain/*anatomy \& histology/*metabolism • Humans
             • *Magnetic Resonance Imaging • Middle Aged •
             Oxygen/metabolism • Prefrontal Cortex/anatomy \&
             histology/metabolism},
   Abstract = {Aging is associated with a decline in both cognitive and
             motor abilities that reflects deterioration of underlying
             brain circuitry. While age-related alterations have also
             been described in brain regions underlying emotional
             behavior (e.g., the amygdala), the functional consequence of
             such changes is less clear. To this end, we used blood
             oxygenation-level dependent (BOLD) functional magnetic
             resonance imaging (fMRI) to explore age-related changes in
             brain regions underlying emotion processing. Twelve young
             (age &lt; 30 years) and 14 elderly subjects (age &gt; 60
             years) were studied with BOLD fMRI during a paradigm that
             involved perceptual processing of fearful and threatening
             stimuli. Consistent with previous reports, direct group
             comparisons revealed relatively increased BOLD fMRI
             responses in prefrontal cortical regions, including Broca's
             area, and relatively decreased responses in the amygdala and
             posterior fusiform gyri in elderly subjects. Importantly,
             additional analyses using an elderly-specific brain template
             for spatial normalization of the elderly BOLD fMRI data
             confirmed these divergent regional response patterns. While
             there was no difference between groups in accuracy on the
             task, elderly subjects were significantly slower (delayed
             reaction times) in performing the task. Our current data
             suggest that elderly subjects engage a more distributed
             neocortical network during the perceptual processing of
             emotional facial expressions. In light of recent converging
             data from two other studies, our observed effects may
             reflect age-related compensatory responses and/or
             alternative strategies in processing emotions, as the
             elderly appear to engage cognitive/linguistic systems in the
             context of reduced sensory and/or limbic
             responses.},
   Language = {eng},
   Doi = {10.1016/j.pscychresns.2005.02.009},
   Key = {Tessitore2005}
}

@article{Brown2005,
   Author = {Brown, SM and Peet, E and Manuck, SB and Williamson, DE and Dahl, RE and Ferrell, RE and Hariri, AR},
   Title = {A regulatory variant of the human tryptophan hydroxylase-2
             gene biases amygdala reactivity},
   Journal = {Molecular Psychiatry},
   Volume = {10},
   Number = {9},
   Pages = {805-},
   Address = {Department of Psychiatry, University of Pittsburgh,
             Pittsburgh, PA 15213, USA.},
   Year = {2005},
   ISSN = {1359-4184},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/16044172},
   Keywords = {Amygdala/*enzymology/physiology • Brain/anatomy \&
             histology/physiology • Emotions/*physiology • Gene
             Frequency • *Genetic Variation • Genotype •
             Humans • Magnetic Resonance Imaging • Oxygen/blood
             • Sequence Deletion • Tryptophan
             Hydroxylase/*genetics},
   Abstract = {Recent studies have indicated that a newly identified second
             isoform of the tryptophan hydroxylase gene (TPH2) is
             preferentially involved in the rate-limiting synthesis of
             neuronal serotonin. Genetic variation in the human TPH2 gene
             (hTPH2) has been associated with altered in vitro enzyme
             activity as well as increased risk for mood disorders. Here,
             we provide the first in vivo evidence that a relatively
             frequent regulatory variant (G(-844)T) of hTPH2 biases the
             reactivity of the amygdala, a neural structure critical in
             the generation and regulation of emotional behaviors. ©
             2005 Nature Publishing Group. All rights
             reserved.},
   Language = {eng},
   Doi = {10.1038/sj.mp.4001725},
   Key = {Brown2005}
}

@article{Pezawas2005,
   Author = {Pezawas, L and Meyer-Lindenberg, A and Drabant, EM and Verchinski,
             BA and Munoz, KE and Kolachana, BS and Egan, MF and Mattay, VS and Hariri,
             AR and Weinberger, DR},
   Title = {5-HTTLPR polymorphism impacts human cingulate-amygdala
             interactions: A genetic susceptibility mechanism for
             depression},
   Journal = {Nature Neuroscience},
   Volume = {8},
   Number = {6},
   Pages = {828-834},
   Address = {Genes, Cognition and Psychosis Program, National Institute
             of Mental Health, National Institutes of Health, 10 Center
             Drive 4S235, Bethesda, Maryland 20892-1379,
             USA.},
   Year = {2005},
   ISSN = {1097-6256},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/15880108},
   Keywords = {Amygdala/*metabolism/pathology/physiopathology •
             Anthropometry • Anxiety Disorders/*genetics/metabolism/pathology
             • Atrophy/genetics/metabolism/pathology • Brain
             Chemistry/genetics • Brain Mapping • Depressive
             Disorder/*genetics/metabolism/pathology •
             Fear/physiology/psychology • Genetic Predisposition to
             Disease/*genetics • Gyrus Cinguli/*metabolism/pathology/physiopathology
             • Humans • Magnetic Resonance Imaging •
             Membrane Glycoproteins/*genetics • Membrane Transport
             Proteins/*genetics • Mutation/genetics • Nerve
             Tissue Proteins/*genetics • Neural Pathways/metabolism/pathology/physiopathology
             • Neuropsychological Tests • Polymorphism,
             Genetic/genetics • Questionnaires •
             Serotonin/metabolism • Serotonin Plasma Membrane
             Transport Proteins},
   Abstract = {Carriers of the short allele of a functional 5′ promoter
             polymorphism of the serotonin transporter gene have
             increased anxiety-related temperamental traits, increased
             amygdala reactivity and elevated risk of depression. Here,
             we used multimodal neuroimaging in a large sample of healthy
             human subjects to elucidate neural mechanisms underlying
             this complex genetic association. Morphometrical analyses
             showed reduced gray matter volume in short-allele carriers
             in limbic regions critical for processing of negative
             emotion, particularly perigenual cingulate and amygdala.
             Functional analysis of those regions during perceptual
             processing of fearful stimuli demonstrated tight coupling as
             a feedback circuit implicated in the extinction of negative
             affect. Short-allele carriers showed relative uncoupling of
             this circuit. Furthermore, the magnitude of coupling
             inversely predicted almost 30% of variation in temperamental
             anxiety. These genotype-related alterations in anatomy and
             function of an amygdala-cingulate feedback circuit critical
             for emotion regulation implicate a developmental,
             systems-level mechanism underlying normal emotional
             reactivity and genetic susceptibility for depression. ©
             2005 Nature Publishing Group.},
   Language = {eng},
   Doi = {10.1038/nn1463},
   Key = {Pezawas2005}
}

@article{Lee2005,
   Author = {Lee, M and Bailer, UF and Frank, GK and Henry, SE and Meltzer, CC and Price, JC and Mathis, CA and Putnam, KT and Ferrell, RE and Hariri, AR and Kaye, WH},
   Title = {Relationship of a 5-HT transporter functional polymorphism
             to 5-HT 1A receptor binding in healthy women
             [1]},
   Journal = {Molecular Psychiatry},
   Volume = {10},
   Number = {8},
   Pages = {715-716},
   Year = {2005},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/15940302},
   Keywords = {Amygdala/physiology • Female • Genotype •
             Humans • Membrane Glycoproteins/*genetics •
             Membrane Transport Proteins/*genetics • Nerve Tissue
             Proteins/*genetics • Neurons/physiology •
             *Polymorphism, Genetic • Receptor, Serotonin,
             5-HT1A/*genetics • Reference Values • Serotonin
             Plasma Membrane Transport Proteins • Statistics,
             Nonparametric},
   Language = {eng},
   Doi = {10.1038/sj.mp.4001680},
   Key = {Lee2005}
}

@article{Hariri2005,
   Author = {Hariri, AR and Drabant, EM and Munoz, KE and Kolachana, BS and Mattay,
             VS and Egan, MF and Weinberger, DR},
   Title = {A susceptibility gene for affective disorders and the
             response of the human amygdala},
   Journal = {Archives of General Psychiatry},
   Volume = {62},
   Number = {2},
   Pages = {146-152},
   Address = {Genes, Cognition and Psychosis Program, National Institute
             of Mental Health Intramural Research Program, National
             Institutes of Health, US Department of Health and Human
             Services, Bethesda, MD 20892, USA.},
   Year = {2005},
   ISSN = {0003-990X},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/15699291},
   Keywords = {Adult • Amygdala/*physiology • Anger/physiology
             • Emotions/*physiology • Facial Expression •
             Fear/physiology • Female • Genetic Predisposition
             to Disease/genetics • Genetic Variation/physiology
             • Genotype • Humans • Magnetic Resonance
             Imaging • Male • Membrane Glycoproteins/*genetics
             • Membrane Transport Proteins/*genetics • Mood
             Disorders/diagnosis/epidemiology/*genetics • Nerve
             Tissue Proteins/*genetics • Oxygen/blood •
             Serotonin Plasma Membrane Transport Proteins • Sex
             Distribution • Stress, Psychological/diagnosis/genetics
             • Transcription, Genetic/physiology • Visual
             Perception/physiology},
   Abstract = {Background: A common regulatory variant (5-HTTLPR) in the
             human serotonin transporter gene (SLC6A4), resulting in
             altered transcription and transporter availability, has been
             associated with vulnerability for affective disorders,
             including anxiety and depression. A recent functional
             magnetic resonance imaging study suggested that this
             association may be mediated by 5-HTTLPR effects on the
             response bias of the human amygdala - a brain region
             critical for emotional and social behavior - to
             environmental threat. Objectives and Design: To examine the
             effects of 5-HTTLPR genotype on the reactivity of the human
             amygdala to salient environmental cues with functional
             magnetic resonance imaging in a large (N = 92) cohort of
             volunteers carefully screened for past and present medical
             or psychiatric illness, and to explore the effects of
             5-HTTLPR genotype as well as amygdala reactivity on harm
             avoidance, a putative personality measure related to trait
             anxiety. Results: We now confirm the finding of 5-HTTLPR
             short allele-driven amygdala hyperreactivity in a large
             independent cohort of healthy subjects with no history of
             psychiatric illness or treatment. Furthermore, we
             demonstrate that these genotype effects on amygdala function
             are consistent with a dominant short allele effect and are
             equally prominent in men and women. However, neither
             5-HTTLPR genotype, amygdala reactivity, nor genotype-driven
             variability in this reactivity was reflected in harm
             avoidance scores. Conclusions: Our results reveal a potent
             modulatory effect of the 5-HTTLPR on amygdala reactivity to
             environmental threat. Since this genetically driven effect
             exists in healthy subjects, it does not, in and of itself,
             predict dimensions of mood or temperament. As such, the
             5-HTTLPR may represent a classic susceptibility factor for
             affective disorders by biasing the functional reactivity of
             the human amygdala in the context of stressful life
             experiences and/or deficient cortical regulatory
             input.},
   Language = {eng},
   Doi = {10.1001/archpsyc.62.2.146},
   Key = {Hariri2005}
}

@article{Meyer-Lindenberg2005,
   Author = {Meyer-Lindenberg, A and Hariri, AR and Munoz, KE and Mervis, CB and Mattay, VS and Morris, CA and Berman, KF},
   Title = {Neural correlates of genetically abnormal social cognition
             in Williams syndrome},
   Journal = {Nature Neuroscience},
   Volume = {8},
   Number = {8},
   Pages = {991-993},
   Address = {Section on Integrative Neuroimaging, National Institute of
             Mental Health, National Institutes of Health, Department of
             Health and Human Services, Bethesda, Maryland 20892, USA.
             andreasml@nih.gov},
   Year = {2005},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/16007084},
   Keywords = {Amygdala/physiopathology • Anxiety/physiopathology
             • Brain/*physiopathology • Brain Mapping •
             Case-Control Studies • *Cognition • Frontal
             Lobe/physiopathology • Humans • *Magnetic
             Resonance Imaging • Prefrontal Cortex/physiopathology
             • *Social Behavior • Williams Syndrome/*physiopathology/*psychology},
   Abstract = {Williams-Beuren syndrome (WBS), caused by a microdeletion of
             approximately 21 genes on chromosome 7q11.23, is
             characterized by unique hypersociability combined with
             increased non-social anxiety. Using functional neuroimaging,
             we found reduced amygdala activation in individuals with WBS
             for threatening faces but increased activation for
             threatening scenes, relative to matched normal controls.
             Activation and interactions of prefrontal regions linked to
             amygdala, especially orbitofrontal cortex, were abnormal,
             suggesting a genetically controlled neural circuitry for
             regulating human social behavior.},
   Language = {eng},
   Doi = {10.1038/nn1494},
   Key = {Meyer-Lindenberg2005}
}

@article{Lerner2005,
   Author = {Lerner, JS and Gonzalez, RM and Dahl, RE and Hariri, AR and Taylor,
             SE},
   Title = {Facial expressions of emotion reveal neuroendocrine and
             cardiovascular stress responses (Retraction in: Biological
             Psychiatry (2007) 61:2 (261))},
   Journal = {Biological Psychiatry},
   Volume = {58},
   Number = {9},
   Pages = {743-750},
   Address = {Department of Social and Decision Sciences, Carnegie Mellon
             University, Pittsburgh, Pennsylvania 15213, USA.
             jlerner@cmu.edu},
   Year = {2005},
   ISSN = {0006-3223},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/16256075},
   Keywords = {Adult • *Cardiovascular Physiological Phenomena •
             Emotions/*physiology • *Facial Expression •
             Fear/physiology/psychology • Female •
             Hemodynamics/physiology • Humans •
             Hydrocortisone/blood • Male • Neurosecretory
             Systems/*physiology • Saliva/metabolism • Stress,
             Psychological/*physiopathology},
   Abstract = {Background: The classic conception of stress involves
             undifferentiated negative affect and corresponding
             biological reactivity. The present study hypothesized a new
             conception that disaggregates stress into emotion-specific,
             contrasting patterns of biological response. Methods:
             Ninety-two healthy adults engaged in stress-challenge tasks,
             during which cardiovascular responses, hypothalamic-pituitary-adrenocortical
             (HPA) axis responses (i.e., cortisol), emotional expressions
             (i.e., facial muscle movements), and subjective emotional
             experience (self-reported) were assessed. Results:
             Pronounced individual differences emerged in specific
             emotional responses to the stressors. Analyses of facial
             expressions revealed that the more fear individuals
             displayed in response to the stressors, the higher their
             cardiovascular and cortisol responses to stress. By
             contrast, the more anger and disgust (indignation)
             individuals displayed in response to the same stressors, the
             lower their cortisol levels and cardiovascular responses.
             Individual differences in optimistic appraisals appeared to
             mediate these correlated patterns. Conclusions: Facial
             expressions of emotion signal biological responses to
             stress. Fear expressions signal elevated cortisol and
             cardiovascular reactivity; anger and disgust signal
             attenuated cortisol and cardiovascular reactivity, patterns
             that implicate individual differences in stress appraisals.
             Rather than conceptualizing stress as generalized negative
             affect, studies can be informed by this emotion-specific
             approach to stress responses. © 2005 Society of Biological
             Psychiatry.},
   Language = {eng},
   Doi = {10.1016/j.biopsych.2005.08.011},
   Key = {Lerner2005}
}

@article{Callicott2005,
   Author = {Callicott, JH and Straub, RE and Pezawas, L and Egan, MF and Mattay, VS and Hariri, AR and Verchinski, BA and Meyer-Lindenberg, A and Balkissoon,
             R and Kolachana, B and Goldberg, TE and Weinberger,
             DR},
   Title = {Variation in DISC1 affects hippocampal structure and
             function and increases risk for schizophrenia},
   Journal = {Proceedings of the National Academy of Sciences of the
             United States of America},
   Volume = {102},
   Number = {24},
   Pages = {8627-8632},
   Address = {Genes, Cognition, and Psychosis Program, Clinical Brain
             Disorders Branch, Division of Intramural Research, National
             Institute of Mental Health, National Institutes of Health,
             Bethesda, MD 20892, USA. callicottj@mail.nih.gov},
   Year = {2005},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/15939883},
   Keywords = {Adult • African Americans • *Alleles •
             European Continental Ancestry Group • Female •
             Haplotypes/genetics • Hippocampus/*anatomy \&
             histology/metabolism/*physiology • Humans •
             Magnetic Resonance Imaging • Male • Nerve Tissue
             Proteins/*genetics/metabolism • Polymorphism, Single
             Nucleotide/genetics • Psychomotor Performance/physiology
             • Risk Factors • Schizophrenia/*genetics},
   Abstract = {Disrupted-in-schizophrenia 1 (DISC1) is a promising
             schizophrenia candidate gene expressed predominantly within
             the hippocampus. We typed 12 single-nucleotide polymorphisms
             (SNPs) that covered the DISC1 gene. A three-SNP haplotype
             [hCV219779 (C)-rs821597 (G)-rs821616 (A)] spanning 83 kb of
             the gene was associated with schizophrenia in a family-based
             sample (P = 0.002). A common nonconservative SNP (Ser704Cys)
             (rs821616) within this haplotype was associated with
             schizophrenia (P = 0.004). Based on primary expression of
             DISC1 in hippocampus, we hypothesized that allelic variation
             at Ser704Cys would have a measurable impact on hippocampal
             structure and function as assayed via specific
             hippocampus-related intermediate phenotypes. In addition to
             overtransmission in schizophrenia, the Ser allele was
             associated with altered hippocampal structure and function
             in healthy subjects, including reduced hippocampal gray
             matter volume and altered engagement of the hippocampus
             during several cognitive tasks assayed with functional
             magnetic resonance imaging. These convergent data suggest
             that allelic variation within DISC1, either at Ser704Cys or
             haplotypes monitored by it, increases the risk for
             schizophrenia and that the mechanism of this effect involves
             structural and functional alterations in the hippocampal
             formation.},
   Language = {eng},
   Doi = {10.1073/pnas.0500515102},
   Key = {Callicott2005}
}

@article{Egan2004,
   Author = {Egan, MF and Straub, RE and Goldberg, TE and Yakub, I and Callicott, JH and Hariri, AR and Mattay, VS and Bertolino, A and Hyde, TM and Shannon-Weickert, C and Akil, M and Crook, J and Vakkalanka, RK and Balkissoon, R and Gibbs, RA and Kleinman, JE and Weinberger,
             DR},
   Title = {Variation in GRM3 affects cognition, prefrontal glutamate,
             and risk for schizophrenia},
   Journal = {Proceedings of the National Academy of Sciences of the
             United States of America},
   Volume = {101},
   Number = {34},
   Pages = {12604-12609},
   Address = {Clinical Brain Disorders Branch, Intramural Research
             Program, National Institute of Mental Health/NIH/DHHS,
             Building 10, Center Drive, Bethesda, MD 20892,
             USA.},
   Year = {2004},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/15310849},
   Keywords = {Adult • Cognition/*physiology • Genetic
             Predisposition to Disease • Genotype •
             Glutamates/*metabolism • Haplotypes •
             Hippocampus/anatomy \& histology/metabolism • Humans
             • Magnetic Resonance Imaging • Middle Aged •
             Neuropsychological Tests • Phenotype • Prefrontal
             Cortex/*metabolism • Receptors, Metabotropic
             Glutamate/genetics/*metabolism • Schizophrenia/*metabolism
             • Sequence Analysis, DNA},
   Abstract = {GRM3, a metabotropic glutamate receptor-modulating synaptic
             glutamate, is a promising schizophrenia candidate gene. In a
             family-based association study, a common GRM3 haplotype was
             strongly associated with schizophrenia (P = 0.0001). Within
             this haplotype, the A allele of single-nucleotide
             polymorphism (SNP) 4 (hCV11245618) in intron 2 was slightly
             overtransmitted to probands (P = 0.02). We studied the
             effects of this SNP on neurobiological traits related to
             risk for schizophrenia and glutamate neurotransmission. The
             SNP4 A allele was associated with poorer performance on
             several cognitive tests of prefrontal and hippocampal
             function. The physiological basis of this effect was
             assessed with functional MRI, which showed relatively
             deleterious activation patterns in both cortical regions in
             control subjects homozygous for the SNP4 A allele. We next
             looked at SNP4's effects on two indirect measures of
             prefrontal glutamate neurotransmission. Prefrontal
             N-acetylaspartate, an in vivo MRI measure related to
             synaptic activity and closely correlated with tissue
             glutamate, was lower in SNP4 AA homozygotes. In postmortem
             human prefrontal cortex, AA homozygotes had lower mRNA
             levels of the glial glutamate transporter EAAT2, a protein
             regulated by GRM3 that critically modulates synaptic
             glutamate. Effects of SNP4 on prefrontal GRM3 mRNA and
             protein levels were marginal. Resequencing revealed no
             missense or splice-site SNPs, suggesting that the intronic
             SNP4 or related haplotypes may exert subtle regulatory
             effects on GRM3 transcription. These convergent data point
             to a specific molecular pathway by which GRM3 genotype
             alters glutamate neurotransmission, prefrontal and
             hippocampal physiology and cognition, and thereby increased
             risk for schizophrenia.},
   Language = {eng},
   Doi = {10.1073/pnas.0405077101},
   Key = {Egan2004}
}

@article{Wang2004,
   Author = {Wang, AT and Dapretto, M and Hariri, AR and Sigman, M and Bookheimer,
             SY},
   Title = {Neural correlates of facial affect processing in children
             and adolescents with autism spectrum disorder},
   Journal = {Journal of the American Academy of Child and Adolescent
             Psychiatry},
   Volume = {43},
   Number = {4},
   Pages = {481-490},
   Address = {Department of Psychology, UCLA, Los Angeles, CA,
             USA.},
   Year = {2004},
   ISSN = {0890-8567},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/15187809},
   Keywords = {Adolescent • Amygdala/*physiopathology • Analysis
             of Variance • Autistic Disorder/*physiopathology •
             Brain Mapping • Case-Control Studies • Cerebral
             Cortex/*physiopathology • Child • Emotions •
             *Facial Expression • Humans • Magnetic Resonance
             Imaging • Male • Psycholinguistics •
             Regression Analysis • *Social Perception},
   Abstract = {Objective: To examine the neural basis of impairments in
             interpreting facial emotions in children and adolescents
             with autism spectrum disorders (ASD). Method: Twelve
             children and adolescents with ASD and 12 typically
             developing (TD) controls matched faces by emotion and
             assigned a label to facial expressions while undergoing
             functional magnetic resonance imaging. Results: Both groups
             engaged similar neural networks during facial emotion
             processing, including activity in the fusiform gyrus (FG)
             and prefrontal cortex. However, between-group analyses in
             regions of interest revealed that when matching facial
             expressions, the ASD group showed significantly less
             activity than the TD group in the FG, but reliably greater
             activity in the precuneus. During the labeling of facial
             emotions, no between-group differences were observed at the
             behavioral or neural level. Furthermore, activity in the
             amygdala was moderated by task demands in the TD group but
             not in the ASD group. Conclusions: These findings suggest
             that children and adolescents with ASD in part recruit
             different neural networks and rely on different strategies
             when processing facial emotions. High-functioning
             individuals with ASD may be relatively unimpaired in the
             cognitive assessment of basic emotions, yet still show
             differences in the automatic processing of facial
             expressions.},
   Language = {eng},
   Doi = {10.1097/00004583-200404000-00015},
   Key = {Wang2004}
}

@article{Hariri2003d,
   Author = {Hariri, A. R. and Goldberg, T. E. and Mattay, V. S. and Kolachana, B. S. and Callicott, J. H. and Egan, M. F. and Weinberger, D. R.},
   Title = {Brain-derived neurotrophic factor val66met polymorphism
             affects human memory-related hippocampal activity and
             predicts memory performance},
   Journal = {The Journal of neuroscience : the official journal of the
             Society for Neuroscience},
   Volume = {23},
   Number = {17},
   Pages = {6690--4},
   Address = {Clinical Brain Disorders Branch, Intramural Research
             Program, National Institute of Mental Health, National
             Institutes of Health, United States Department of Health and
             Human Services, Bethesda, Maryland 20892-1384,
             USA.},
   Year = {2003},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/12890761},
   Keywords = {Adult • Amino Acid Substitution/*genetics •
             Brain/anatomy \& histology/physiology • Brain Mapping
             • Brain-Derived Neurotrophic Factor/*genetics •
             Cohort Studies • DNA Mutational Analysis • Female
             • Genotype • Heterozygote •
             Hippocampus/anatomy \& histology/*physiology •
             Homozygote • Humans • Magnetic Resonance Imaging
             • Male • Memory/*physiology • Photic
             Stimulation • Polymorphism, Genetic/*genetics •
             Reference Values • Regression Analysis},
   Abstract = {BDNF plays a critical role in activity-dependent
             neuroplasticity underlying learning and memory in the
             hippocampus. A frequent single nucleotide polymorphism in
             the targeting region of the human BDNF gene (val66met) has
             been associated with abnormal intracellular trafficking and
             regulated secretion of BDNF in cultured hippocampal neurons
             transfected with the met allele. In addition, the met allele
             has been associated with abnormal hippocampal neuronal
             function as well as impaired episodic memory in human
             subjects, but a direct effect of BDNF alleles on hippocampal
             processing of memory has not been demonstrated. We studied
             the relationship of the BDNF val66met genotype and
             hippocampal activity during episodic memory processing using
             blood oxygenation level-dependent functional magnetic
             resonance imaging and a declarative memory task in healthy
             individuals. Met carriers exhibited relatively diminished
             hippocampal engagement in comparison with val homozygotes
             during both encoding and retrieval processes. Remarkably,
             the interaction between the BDNF val66met genotype and the
             hippocampal response during encoding accounted for 25\% of
             the total variation in recognition memory performance. These
             data implicate a specific genetic mechanism for substantial
             normal variation in human declarative memory and suggest
             that the basic effects of BDNF signaling on hippocampal
             function in experimental animals are important in
             humans.},
   Language = {eng},
   Key = {Hariri2003d}
}

@article{Mattay2003,
   Author = {Mattay, V. S. and Goldberg, T. E. and Fera, F. and Hariri,
             A. R. and Tessitore, A. and Egan, M. F. and Kolachana, B. and Callicott, J. H. and Weinberger, D. R.},
   Title = {Catechol O-methyltransferase val158-met genotype and
             individual variation in the brain response to
             amphetamine},
   Journal = {Proceedings of the National Academy of Sciences of the
             United States of America},
   Volume = {100},
   Number = {10},
   Pages = {6186--91},
   Address = {Clinical Brain Disorders Branch, National Institute of
             Mental Health, National Institutes of Health, Department of
             Health and Human Services, Building 10, Center Drive, Room
             4S-235, Bethesda, MD 20982-1379, USA.},
   Year = {2003},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/12716966},
   Keywords = {Amino Acid Substitution • Brain/drug
             effects/enzymology/*physiology • Catechol
             O-Methyltransferase/*genetics • DNA/genetics/isolation
             \& purification • Dextroamphetamine/*pharmacology
             • Genotype • Humans • Magnetic Resonance
             Imaging • Methionine • Organ Specificity •
             Valine},
   Abstract = {Monamines subserve many critical roles in the brain, and
             monoaminergic drugs such as amphetamine have a long history
             in the treatment of neuropsychiatric disorders and also as a
             substance of abuse. The clinical effects of amphetamine are
             quite variable, from positive effects on mood and cognition
             in some individuals, to negative responses in others,
             perhaps related to individual variations in monaminergic
             function and monoamine system genes. We explored the effect
             of a functional polymorphism (val(158)-met) in the catechol
             O-methyltransferase gene, which has been shown to modulate
             prefrontal dopamine in animals and prefrontal cortical
             function in humans, on the modulatory actions of amphetamine
             on the prefrontal cortex. Amphetamine enhanced the
             efficiency of prefrontal cortex function assayed with
             functional MRI during a working memory task in subjects with
             the high enzyme activity val/val genotype, who presumably
             have relatively less prefrontal synaptic dopamine, at all
             levels of task difficulty. In contrast, in subjects with the
             low activity met/met genotype who tend to have superior
             baseline prefrontal function, the drug had no effect on
             cortical efficiency at low-to-moderate working memory load
             and caused deterioration at high working memory load. These
             data illustrate an application of functional neuroimaging in
             pharmacogenomics and extend basic evidence of an
             inverted-``U'' functional-response curve to increasing
             dopamine signaling in the prefrontal cortex. Further,
             individuals with the met/met catechol O-methyltransferase
             genotype appear to be at increased risk for an adverse
             response to amphetamine.},
   Language = {eng},
   Doi = {10.1073/pnas.0931309100},
   Key = {Mattay2003}
}

@article{Hariri2003c,
   Author = {Hariri, AR and Mattay, VS and Tessitore, A and Fera, F and Weinberger,
             DR},
   Title = {Neocortical modulation of the amygdala response to fearful
             stimuli},
   Journal = {Biological Psychiatry},
   Volume = {53},
   Number = {6},
   Pages = {494-501},
   Address = {Clinical Brain Disorders Branch, Intramural Research
             Program, National Institute of Mental Health, National
             Institutes of Health, Department of Health and Human
             Services, Bethesda, Maryland 20892, USA.},
   Year = {2003},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/12644354},
   Keywords = {Adult • Affect • Amygdala/*anatomy \&
             histology/*metabolism • Cognition/physiology •
             Equipment Design • *Fear • Female • Galvanic
             Skin Response/physiology • Humans • Magnetic
             Resonance Imaging/instrumentation • Male •
             Oxygen/blood • Photic Stimulation • Prefrontal
             Cortex/*anatomy \& histology/*metabolism},
   Abstract = {Background: The cortical circuitry involved in conscious
             cognitive processes and the subcortical circuitry involved
             in fear responses have been extensively studied with
             neuroimaging, but their interactions remain largely
             unexplored. A recent functional magnetic resonance imaging
             (fMRI) study demonstrated that the engagement of the right
             prefrontal cortex during the cognitive evaluation of angry
             and fearful facial expressions is associated with an
             attenuation of the response of the amygdala to these same
             stimuli, providing evidence for a functional neural network
             for emotional regulation. Methods: In the current study, we
             have explored the generalizability of this functional
             network by using threatening and fearful non-face stimuli
             derived from the International Affective Picture System
             (IAPS), as well as the influence of this network on
             peripheral autonomic responses. Results: Similar to the
             earlier findings with facial expressions, blood oxygen level
             dependent fMRI revealed that whereas perceptual processing
             of IAPS stimuli was associated with a bilateral amygdala
             response, cognitive evaluation of these same stimuli was
             associated with attenuation of this amygdala response and a
             correlated increase in response of the right prefrontal
             cortex and the anterior cingulate cortex. Moreover, this
             pattern was reflected in changes in skin conductance.
             Conclusions: The current results further implicate the
             importance of neocortical regions, including the prefrontal
             and anterior cingulate cortices, in regulating emotional
             responses mediated by the amygdala through conscious
             evaluation and appraisal. © 2003 Society of Biological
             Psychiatry.},
   Language = {eng},
   Doi = {10.1016/S0006-3223(02)01786-9},
   Key = {Hariri2003c}
}

@article{Holmes2003,
   Author = {Holmes, A and Hariri, AR},
   Title = {The serotonin transporter gene-linked polymorphism and
             negative emotionality: Placing single gene effects in the
             context of genetic background and environment},
   Journal = {Genes, Brain and Behavior},
   Volume = {2},
   Number = {6},
   Pages = {332-335},
   Year = {2003},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/14653304},
   Keywords = {Animals • Brain/physiopathology • Carrier
             Proteins/*genetics • Disease Models, Animal •
             Emotions/*physiology • Environment • Humans •
             Membrane Glycoproteins/*genetics • *Membrane Transport
             Proteins • Mice • Mood Disorders/*genetics •
             *Nerve Tissue Proteins • Polymorphism,
             Genetic/*physiology • Promoter Regions,
             Genetic/*genetics • Serotonin • Serotonin Plasma
             Membrane Transport Proteins},
   Language = {eng},
   Doi = {10.1046/j.1601-1848.2003.00052.x},
   Key = {Holmes2003}
}

@article{Hariri2003b,
   Author = {Hariri, AR and Weinberger, DR},
   Title = {Functional neuroimaging of genetic variation in serotonergic
             neurotransmission},
   Journal = {Genes, Brain and Behavior},
   Volume = {2},
   Number = {6},
   Pages = {341-349},
   Address = {Clinical Brain Disorders Branch, Intramural Research
             Program, National Institute of Mental Health, National
             Institutes of Health, US Department of Health and Human
             Services, Bethesda, Maryland, USA. haririar@upmc.edu},
   Year = {2003},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/14653306},
   Keywords = {Amygdala/*physiology • Animals • *Brain Mapping
             • Fear/physiology • Genetic Variation •
             Humans • *Magnetic Resonance Imaging • Nerve
             Net/physiology • Neural Pathways/physiology •
             Polymorphism, Genetic/*genetics • Serotonin/*genetics
             • Synaptic Transmission/*genetics},
   Abstract = {Serotonin (5-hydroxytryptamine; 5-HT) is a potent modulator
             of the physiology and behavior involved in generating
             appropriate responses to environmental cues such as danger
             or threat. Furthermore, genetic variation in 5-HT subsystem
             genes can impact upon several dimensions of emotional
             behavior including neuroticism and psychopathology, but
             especially anxiety traits. Recently, functional neuroimaging
             has provided a dramatic illustration of how a promoter
             polymorphism in the human 5-HT transporter (5-HTT) gene,
             which has been weakly related to these behaviors, is
             strongly related to the engagement of neural systems, namely
             the amygdala, subserving emotional processes. In this
             commentary, we discuss how functional neuroimaging can be
             used to characterize the effects of polymorphisms in 5-HT
             subsystem genes on the response of neural circuits
             underlying the generation and regulation of mood and
             temperament as well as susceptibility to affective illness.
             We argue that in time, such knowledge will allow us to not
             only transcend phenomenological diagnosis and represent
             mechanisms of disease, but also identify at-risk individuals
             and biological pathways for the development of new
             treatments.},
   Language = {eng},
   Doi = {10.1046/j.1601-1848.2003.00048.x},
   Key = {Hariri2003b}
}

@article{fds252077,
   Author = {Mattay, VS and Goldberg, TE and Fera, F and Hariri, AR and Tessitore, A and Egan, MF and Kolachana, B and Callicott, JH and Weinberger,
             DR},
   Title = {Catechol O-methyltransferase val158-met genotype
             and individual variation in the brain response to
             amphetamine},
   Journal = {Proceedings of the National Academy of Sciences of
             USA},
   Volume = {100},
   Number = {10},
   Pages = {6186-6191},
   Year = {2003},
   ISSN = {0027-8424},
   url = {http://dx.doi.org/10.1073/pnas.0931309100},
   Abstract = {Monamines subserve many critical roles in the brain, and
             monoaminergic drugs such as amphetamine have a long history
             in the treatment of neuropsychiatric disorders and also as a
             substance of abuse. The clinical effects of amphetamine are
             quite variable, from positive effects on mood and cognition
             in some individuals, to negative responses in others,
             perhaps related to individual variations in monaminergic
             function and monoamine system genes. We explored the effect
             of a functional polymorphism (val158-met) in the catechol
             O-methyltransferase gene, which has been shown to modulate
             prefrontal dopamine in animals and prefrontal cortical
             function in humans, on the modulatory actions of amphetamine
             on the prefrontal cortex. Amphetamine enhanced the
             efficiency of prefrontal cortex function assayed with
             functional MRI during a working memory task in subjects with
             the high enzyme activity val/val genotype, who presumably
             have relatively less prefrontal synaptic dopamine, at all
             levels of task difficulty. In contrast, in subjects with the
             low activity met/met genotype who tend to have superior
             baseline prefrontal function, the drug had no effect on
             cortical efficiency at low-to-moderate working memory load
             and caused deterioration at high working memory load. These
             data illustrate an application of functional neuroimaging in
             pharmacogenomics and extend basic evidence of an
             inverted-"U" functional-response curve to increasing
             dopamine signaling in the prefrontal cortex. Further,
             individuals with the met/met catechol O-methyltransferase
             genotype appear to be at increased risk for an adverse
             response to amphetamine.},
   Doi = {10.1073/pnas.0931309100},
   Key = {fds252077}
}

@article{Hariri2003a,
   Author = {Hariri, AR and Weinberger, DR},
   Title = {Imaging genomics},
   Journal = {British Medical Bulletin},
   Volume = {65},
   Pages = {259-270},
   Address = {Clinical Brain Disorders Branch, Intramural Research
             Program, National Institute of Mental Health, National
             Institutes of Health, Bethesda, Maryland 20892,
             USA.},
   Year = {2003},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/12697630},
   Keywords = {Apolipoproteins E/genetics • Brain/*pathology •
             Brain Diseases/*genetics/pathology • Carrier
             Proteins/genetics • Catechol O-Methyltransferase/genetics
             • *Genomics • Humans • *Magnetic Resonance
             Imaging • Membrane Glycoproteins/genetics •
             *Membrane Transport Proteins • *Nerve Tissue Proteins
             • Polymorphism, Genetic • Serotonin Plasma
             Membrane Transport Proteins},
   Abstract = {The recent completion of a working draft of the human genome
             sequence promises to provide unprecedented opportunities to
             explore the genetic basis of individual differences in
             complex behaviours and vulnerability to neuropsychiatric
             illness. Functional neuroimaging, because of its unique
             ability to assay information processing at the level of
             brain within individuals, provides a powerful approach to
             such functional genomics. Recent fMRI studies have
             established important physiological links between functional
             genetic polymorphisms and robust differences in information
             processing within distinct brain regions and circuits that
             have been linked to the manifestation of various disease
             states such as Alzheimer's disease, schizophrenia and
             anxiety disorders. Importantly, all of these biological
             relationships have been revealed in relatively small samples
             of healthy volunteers and in the absence of observable
             differences at the level of behaviour, underscoring the
             power of a direct assay of brain physiology like fMRI in
             exploring the functional impact of genetic
             variation.},
   Language = {eng},
   Doi = {10.1093/bmb/65.1.259},
   Key = {Hariri2003a}
}

@article{fds252120,
   Author = {Hariri, AR and Goldberg, TE and Mattay, VS and Kolachana, BS and Callicott, JH and Egan, MF and Weinberger, DR},
   Title = {Brain-derived neurotrophic factor val66met
             polymorphism affects human memory-related hippocampal
             activity and predicts memory performance},
   Journal = {Journal of Neuroscience},
   Volume = {23},
   Number = {17},
   Pages = {6690-6694},
   Year = {2003},
   Abstract = {BDNF plays a critical role in activity-dependent
             neuroplasticity underlying learning and memory in the
             hippocampus. A frequent single nucleotide polymorphism in
             the targeting region of the human BDNF gene (val66met) has
             been associated with abnormal intracellular trafficking and
             regulated secretion of BDNF in cultured hippocampal neurons
             transfected with the met allele. In addition, the met allele
             has been associated with abnormal hippocampal neuronal
             function as well as impaired episodic memory in human
             subjects, but a direct effect of BDNF alleles on hippocampal
             processing of memory has not been demonstrated. We studied
             the relationship of the BDNF val66Met genotype and
             hippocampal activity during episodic memory processing using
             blood oxygenation level-dependent functional magnetic
             resonance imaging and a declarative memory task in healthy
             individuals. Met carriers exhibited relatively diminished
             hippocampal engagement in comparison with val homozygotes
             during both encoding and retrieval processes. Remarkably,
             the interaction between the BDNF val66met genotype and the
             hippocampal response during encoding accounted for 25% of
             the total variation in recognition memory performance. These
             data implicate a specific genetic mechanism for substantial
             normal variation in human declarative memory and suggest
             that the basic effects of BDNF signaling on hippocampal
             function in experimental animals are important in
             humans.},
   Key = {fds252120}
}

@article{fds251988,
   Author = {Tessitore, A and Hariri, AR and Fera, F and Smith, WG and Chase, TN and Hyde, TM and Weinberger, DR and Mattay, VS},
   Title = {Erratum: Dopamine modulates the response of the human
             amygdala: A study in Parkinson's disease (Journal of
             Neuroscience (October 15, 2002) (9099-9103))},
   Journal = {Journal of Neuroscience},
   Volume = {22},
   Number = {24},
   Pages = {i},
   Year = {2002},
   Key = {fds251988}
}

@article{Tessitore2002,
   Author = {Tessitore, A and Hariri, AR and Fera, F and Smith, WG and Chase, TN and Hyde, TM and Weinberger, DR and Mattay, VS},
   Title = {Dopamine modulates the response of the human amygdala: A
             study in Parkinson's disease},
   Journal = {Journal of Neuroscience},
   Volume = {22},
   Number = {20},
   Pages = {9099-9103},
   Address = {Clinical Brain Disorders Branch, National Institute of
             Mental Health, National Institutes of Health, Bethesda,
             Maryland 20892-1384, USA.},
   Year = {2002},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/12388617},
   Keywords = {Amygdala/drug effects/*physiopathology • Antiparkinson
             Agents/therapeutic use • Behavior • Brain Mapping
             • Dopamine/*metabolism/pharmacology • Dopamine
             Agonists/therapeutic use • Drug Therapy, Combination
             • Emotions/physiology • Facial Expression •
             Female • Humans • Magnetic Resonance Imaging
             • Male • Middle Aged • Parkinson
             Disease/*physiopathology • Pattern Recognition, Visual
             • Photic Stimulation • Reaction Time •
             Reference Values},
   Abstract = {In addition to classic motor signs and symptoms, Parkinson's
             disease (PD) is characterized by neuropsychological and
             emotional deficits, including a blunted emotional response.
             In the present study, we explored both the neural basis of
             abnormal emotional behavior in PD and the physiological
             effects of dopaminergic therapy on the response of the
             amygdala, a central structure in emotion processing. PD
             patients and matched normal controls (NCs) were studied with
             blood oxygenation level-dependent functional magnetic
             resonance imaging during a paradigm that involved perceptual
             processing of fearful stimuli. PD patients were studied
             twice, once during a relatively hypodopaminergic state
             (i.e., ≥12 hr after their last dose of dopamimetic
             treatment) and again during a dopamine-replete state. The
             imaging data revealed a robust bilateral amygdala response
             in NCs that was absent in PD patients during the
             hypodopaminergic state. Dopamine repletion partially
             restored this response in PD patients. Our results
             demonstrate an abnormal amygdala response in PD that may
             underlie the emotional deficits accompanying the disease.
             Furthermore, consistent with findings in experimental animal
             paradigms, our results provide in vivo evidence of the role
             of dopamine in modulating the response of the amygdala to
             sensory information in human subjects.},
   Language = {eng},
   Key = {Tessitore2002}
}

@article{Hariri2002a,
   Author = {Hariri, AR and Tessitore, A and Mattay, VS and Fera, F and Weinberger,
             DR},
   Title = {The amygdala response to emotional stimuli: A comparison of
             faces and scenes},
   Journal = {NeuroImage},
   Volume = {17},
   Number = {1},
   Pages = {317-323},
   Address = {Clinical Brain Disorders Branch, Intramural Research
             Program, National Institute of Mental Health, National
             Institutes of Health, Bethesda, Maryland 20892, USA.
             hariria@intra.nimh.nih.gov},
   Year = {2002},
   ISSN = {1053-8119},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/12482086},
   Keywords = {Adult • Amygdala/anatomy \& histology/*physiology
             • Anger/physiology • Emotions/*physiology •
             *Facial Expression • Fear/physiology • Female
             • Galvanic Skin Response/physiology • Humans
             • Image Interpretation, Computer-Assisted •
             Individuality • Magnetic Resonance Imaging • Male
             • Reaction Time/physiology • Social
             Perception},
   Abstract = {As a central fear processor of the brain, the amygdala
             initiates a cascade of critical physiological and behavioral
             responses. Neuroimaging studies have shown that the human
             amygdala responds not only to fearful and angry facial
             expressions but also to fearful and threatening scenes such
             as attacks, explosions, and mutilations. Given the relative
             importance of facial expressions in adaptive social
             behavior, we hypothesized that the human amygdala would
             exhibit a stronger response to angry and fearful facial
             expressions in comparison to other fearful and threatening
             stimuli. Twelve subjects completed two tasks while
             undergoing fMRI: matching angry or fearful facial
             expressions, and matching scenes depicting fearful or
             threatening situations derived from the International
             Affective Picture System (IAPS). While there was an amygdala
             response to both facial expressions and IAPS stimuli, direct
             comparison revealed that the amygdala response to facial
             expressions was significantly greater than that to IAPS
             stimuli. Autonomic reactivity, measured by skin conductance
             responses, was also greater to facial expressions. These
             results suggest that the human amygdala shows a stronger
             response to affective facial expressions than to scenes, a
             bias that should be considered in the design of experimental
             paradigms interested in probing amygdala
             function.},
   Language = {eng},
   Doi = {10.1006/nimg.2002.1179},
   Key = {Hariri2002a}
}

@article{Mattay2002,
   Author = {Mattay, VS and Fera, F and Tessitore, A and Hariri, AR and Das, S and Callicott, JH and Weinberger, DR},
   Title = {Neurophysiological correlates of age-related changes in
             human motor function},
   Journal = {Neurology},
   Volume = {58},
   Number = {4},
   Pages = {630-635},
   Address = {Clinical Brain Disorders Branch, Intramural Research
             Program, National Institute of Mental Health, NIH, Bethesda,
             MD 20892-1379, USA. vsm@helix.nih.gov},
   Year = {2002},
   ISSN = {0028-3878},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/11865144},
   Keywords = {Adult • Aging/*physiology • Analysis of Variance
             • Brain/*physiology • Female • Humans •
             Magnetic Resonance Imaging/statistics \& numerical data
             • Male • Middle Aged • Psychomotor
             Performance/*physiology},
   Abstract = {Background: There are well-defined and characteristic
             age-related deficits in motor abilities that may reflect
             structural and chemical changes in the aging brain.
             Objective: To delineate age-related changes in the
             physiology of brain systems subserving simple motor
             behavior. Methods: Ten strongly right-handed young (&lt;35
             years of age) and 12 strongly right-handed elderly (&gt;50
             years of age) subjects with no evidence of cognitive or
             motor deficits participated in the study. Whole-brain
             functional imaging was performed on a 1.5-T MRI scanner
             using a spiral pulse sequence while the subjects performed a
             visually paced "button-press" motor task with their dominant
             right hand alternating with a rest state. Results: Although
             the groups did not differ in accuracy, there was an increase
             in reaction time in the elderly subjects (mean score ± SD,
             young subjects = 547 ± 97 ms, elderly subjects = 794 ± 280
             ms, p &lt; 0.03). There was a greater extent of activation
             in the contralateral sensorimotor cortex, lateral premotor
             area, supplementary motor area, and ipsilateral cerebellum
             in the elderly subjects relative to the young subjects (p
             &lt; 0.001). Additional areas of activation, absent in the
             young subjects, were seen in the ipsilateral sensorimotor
             cortex, putamen (left &gt; right), and contralateral
             cerebellum of the elderly subjects. Conclusions: The results
             of this study show that elderly subjects recruit additional
             cortical and subcortical areas even for the performance of a
             simple motor task. These changes may represent compensatory
             mechanisms invoked by the aging brain, such as
             reorganization and redistribution of functional networks to
             compensate for age-related structural and neurochemical
             changes.},
   Language = {eng},
   Key = {Mattay2002}
}

@article{Hariri2002c,
   Author = {Hariri, AR and Mattay, VS and Tessitore, A and Fera, F and Smith, WG and Weinberger, DR},
   Title = {Dextroamphetamine modulates the response of the human
             amygdala},
   Journal = {Neuropsychopharmacology},
   Volume = {27},
   Number = {6},
   Pages = {1036-1040},
   Address = {Clinical Brain Disorders Branch, Intramural Research
             Program, National Institute of Mental Health, National
             Institutes of Health, Bethesda, MD, USA.
             hariria@intra.nimh.nih.gov},
   Year = {2002},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/12464460},
   Keywords = {Adult • Amygdala/*drug effects/physiology •
             Dextroamphetamine/*pharmacology • Double-Blind Method
             • Emotions/*drug effects/physiology • Facial
             Expression • Female • Humans • Magnetic
             Resonance Imaging/methods/statistics \& numerical data
             • Male},
   Abstract = {Amphetamine, a potent monoaminergic agonist, has pronounced
             effects on emotional behavior in humans, including the
             generation of fear and anxiety. Recent animal studies have
             demonstrated the importance of monoamines, especially
             dopamine, in modulating the response of the amygdala, a key
             brain region involved in the perception of fearful and
             threatening stimuli, and the generation of appropriate
             physiological and behavioral responses. We have explored the
             possibility that the anxiogenic effect of amphetamine in
             humans reflects the drug's influence on the activity of the
             amygdala. In a double-blind placebo controlled study, fMRI
             revealed that dextroamphetamine potentiated the response of
             the amygdala during the perceptual processing of angry and
             fearful facial expressions. Our results provide the first
             evidence of a specific neural substrate for the anxiogenic
             effects of amphetamine and are consistent with animal models
             of dopaminergic activation of the amygdala. © 2002 American
             College of Neuropsychopharmacology. Published by Elsevier
             Science Inc.},
   Language = {eng},
   Doi = {10.1016/S0893-133X(02)00373-1},
   Key = {Hariri2002c}
}

@article{Hariri2002b,
   Author = {Hariri, AR and Mattay, VS and Tessitore, A and Kolachana, B and Fera, F and Goldman, D and Egan, MF and Weinberger, DR},
   Title = {Serotonin transporter genetic variation and the response of
             the human amygdala},
   Journal = {Science},
   Volume = {297},
   Number = {5580},
   Pages = {400-403},
   Address = {Clinical Brain Disorders Branch, Intramural Research
             Program, National Institute of Mental Health, National
             Institutes of Health, Bethesda, MD 20892,
             USA.},
   Year = {2002},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/12130784},
   Keywords = {Adult • Alleles • Amygdala/*physiology •
             Carrier Proteins/*genetics/physiology • Cohort Studies
             • Facial Expression • *Fear • Female •
             Functional Laterality • *Genetic Variation •
             Genotype • Humans • Magnetic Resonance Imaging
             • Male • Membrane Glycoproteins/*genetics/physiology
             • *Membrane Transport Proteins • *Nerve Tissue
             Proteins • Personality • Polymorphism, Genetic
             • *Promoter Regions, Genetic •
             Serotonin/*metabolism • Serotonin Plasma Membrane
             Transport Proteins • Sex Characteristics},
   Abstract = {A functional polymorphism in the promoter region of the
             human serotonin transporter gene (SLC6A4) has been
             associated with several dimensions of neuroticism and
             psychopathology, especially anxiety traits, but the
             predictive value of this genotype against these complex
             behaviors has been inconsistent. Serotonin
             [5-hydroxytryptamine, (5-HT)] function influences normal
             fear as well as pathological anxiety, behaviors critically
             dependent on the amygdala in animal models and in clinical
             studies. We now report that individuals with one or two
             copies of the short allele of the serotonin transporter
             (5-HTT) promoter polymorphism, which has been associated
             with reduced 5-HTT expression and function and increased
             fear and anxiety-related behaviors, exhibit greater amygdala
             neuronal activity, as assessed by BOLD functional magnetic
             resonance imaging, in response to fearful stimuli compared
             with individuals homozygous for the long allele. These
             results demonstrate genetically driven variation in the
             response of brain regions underlying human emotional
             behavior and suggest that differential excitability of the
             amygdala to emotional stimuli may contribute to the
             increased fear and anxiety typically associated with the
             short SLC6A4 allele.},
   Language = {eng},
   Doi = {10.1126/science.1071829},
   Key = {Hariri2002b}
}

@article{fds304681,
   Author = {Hale, TS and Hariri, AR and McCracken, JT},
   Title = {Attention-deficit/hyperactivity disorder: Perspectives from
             neuroimaging},
   Journal = {Mental Retardation and Developmental Disabilities Research
             Reviews},
   Volume = {6},
   Number = {3},
   Pages = {214-219},
   Year = {2000},
   ISSN = {1080-4013},
   url = {http://dx.doi.org/10.1002/1098-2779(2000)6:3<214::AID-MRDD9>3.0.CO;2-M},
   Abstract = {Attention-deficit/hyperactivity disorder (ADHD) is a common
             childhood behavioral disorder most often characterized by
             inattentiveness, impulsivity, and hyperactivity. Current
             etiologic theories suggest that ADHD stems from
             abnormalities in dopaminergic and possibly noradrenergic
             brainstem nuclei that act to regulate a cortico-striato-thalamo-cortical
             network, believed to be critical for executive functions and
             the regulation of behavioral responses such as arousal,
             attention, and inhibition. Noninvasive structural and
             functional neuroimaging techniques provide a new avenue for
             exploring the validity of these theories. Despite their
             limitations, neuroimaging studies have provided a unique and
             otherwise inaccessible, biological perspective of ADHD.
             Collectively, the studies reviewed here reveal that
             dysfunction in arousal, behavioral inhibition, and attention
             associated with ADHD may result from structural
             abnormalities in frontostriatal regions that in turn result
             in diminished activity essential for normal function. (C)
             2000 Wiley-Liss, Inc.},
   Doi = {10.1002/1098-2779(2000)6:3<214::AID-MRDD9>3.0.CO;2-M},
   Key = {fds304681}
}

@article{fds252009,
   Author = {Hariri, A and Sigman, M and Bookheimer, S},
   Title = {Abnormal regional brain activity associated with processing
             emotional stimuli in autistic subjects},
   Journal = {NeuroImage},
   Volume = {11},
   Number = {5 PART II},
   Pages = {S242},
   Year = {2000},
   Key = {fds252009}
}

@article{Hale2000,
   Author = {Hale, TS and Hariri, AR and McCracken, JT},
   Title = {Attention-deficit/hyperactivity disorder: perspectives from
             neuroimaging},
   Journal = {Mental retardation and developmental disabilities research
             reviews},
   Volume = {6},
   Number = {3},
   Pages = {214-219},
   Address = {UCLA School of Medicine, Los Angeles, California 90024,
             USA.},
   Year = {2000},
   ISSN = {1080-4013},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/10982499},
   Keywords = {Attention Deficit Disorder with Hyperactivity/*pathology/physiopathology
             • Brain/*pathology/radiography/radionuclide imaging
             • Electroencephalography • Humans • Magnetic
             Resonance Imaging • Tomography, Emission-Computed,
             Single-Photon • Tomography, X-Ray Computed},
   Abstract = {Attention-deficit/hyperactivity disorder (ADHD) is a common
             childhood behavioral disorder most often characterized by
             inattentiveness, impulsivity, and hyperactivity. Current
             etiologic theories suggest that ADHD stems from
             abnormalities in dopaminergic and possibly noradrenergic
             brainstem nuclei that act to regulate a cortico-striato-thalamo-cortical
             network, believed to be critical for executive functions and
             the regulation of behavioral responses such as arousal,
             attention, and inhibition. Noninvasive structural and
             functional neuroimaging techniques provide a new avenue for
             exploring the validity of these theories. Despite their
             limitations, neuroimaging studies have provided a unique and
             otherwise inaccessible, biological perspective of ADHD.
             Collectively, the studies reviewed here reveal that
             dysfunction in arousal, behavioral inhibition, and attention
             associated with ADHD may result from structural
             abnormalities in frontostriatal regions that in turn result
             in diminished activity essential for normal
             function.},
   Language = {eng},
   Doi = {10.1002/1098-2779(2000)6:33.0.CO;2-M},
   Key = {Hale2000}
}

@article{Hariri2000,
   Author = {Hariri, AR and Bookheimer, SY and Mazziotta, JC},
   Title = {Modulating emotional responses: Effects of a neocortical
             network on the limbic system},
   Journal = {NeuroReport},
   Volume = {11},
   Number = {1},
   Pages = {43-48},
   Address = {Brain Mapping Division, UCLA School of Medicine,
             Ahmanson-Lovelace Brain Mapping Center 90095,
             USA.},
   Year = {2000},
   ISSN = {0959-4965},
   url = {http://www.ncbi.nlm.nih.gov/pubmed/10683827},
   Keywords = {Adult • Amygdala/blood supply/physiology •
             Anger/physiology • Cerebrovascular Circulation/physiology
             • Emotions/*physiology • Facial Expression •
             Fear/physiology • Female • Humans • Image
             Interpretation, Computer-Assisted • Limbic System/blood
             supply/*physiology • Magnetic Resonance Imaging •
             Male • Neocortex/blood supply/*physiology • Nerve
             Net/*physiology • Social Perception},
   Abstract = {Humans share with animals a primitive neural system for
             processing emotions such as fear and anger. Unlike other
             animals, humans have the unique ability to control and
             modulate instinctive emotional reactions through
             intellectual processes such as reasoning, rationalizing, and
             labeling our experiences. This study used functional MRI to
             identify the neural networks underlying this ability.
             Subjects either matched the affect of one of two faces to
             that of a simultaneously presented target face (a perceptual
             task) or identified the affect of a target face by choosing
             one of two simultaneously presented linguistic labels (an
             intellectual task). Matching angry or frightened expressions
             was associated with increased regional cerebral blood flow
             (rCBF) in the left and right amygdala, the brain's primary
             fear centers. Labeling these same expressions was associated
             with a diminished rCBF response in the amygdalae. This
             decrease correlated with a simultaneous increase in rCBF in
             the right prefrontal cortex, a neocortical region implicated
             in regulating emotional responses. These results provide
             evidence for a network in which higher regions attenuate
             emotional responses at the most fundamental levels in the
             brain and suggest a neural basis for modulating emotional
             experience through interpretation and labeling.},
   Language = {eng},
   Key = {Hariri2000}
}

@article{fds252007,
   Author = {Dapretto, M and Hariri, A and Bialik, MH and Bookheimer,
             SY},
   Title = {Cortical correlates of affective vs. linguistic prosody: An
             fMRI study},
   Journal = {NeuroImage},
   Volume = {9},
   Number = {6 PART II},
   Pages = {S1054},
   Year = {1999},
   ISSN = {1053-8119},
   Key = {fds252007}
}

@article{fds252008,
   Author = {Hariri, A and Quintana, J and Kovalik, E and Bookheimer,
             S},
   Title = {Processing of facial affect in schizophrenics: An fMRI
             study},
   Journal = {NeuroImage},
   Volume = {9},
   Number = {6 PART II},
   Pages = {S647},
   Year = {1999},
   ISSN = {1053-8119},
   Key = {fds252008}
}

@article{fds252005,
   Author = {Bookheimer, SY and Zeineh, MM and Strojwas, MH and Hariri,
             AR},
   Title = {Localization of memory-related activation on a picture
             priming task using fMRI},
   Journal = {NeuroImage},
   Volume = {7},
   Number = {4 PART II},
   Pages = {S824},
   Year = {1998},
   Key = {fds252005}
}

@article{fds252006,
   Author = {Hariri, AR and Werren, JH and Wilkinson, GS},
   Title = {Distribution and reproductive effects of Wolbachia in
             stalk-eyed flies (Diptera: Diopsidae)},
   Journal = {Heredity},
   Volume = {81},
   Number = {3},
   Pages = {254-260},
   Year = {1998},
   url = {http://dx.doi.org/10.1038/sj.hdy.6883640},
   Abstract = {Wolbachia are cytoplasmically inherited bacteria capable of
             altering the reproductive biology of their hosts in a manner
             which increases their spread within a population. These
             microbes can cause cytoplasmic incompatibility,
             parthenogenesis and feminization of genetic males. Because
             Wolbachia have been associated with female-biased sex ratio
             distortion, we used a PCR assay to examine 17 species of
             stalk-eyed flies (Diptera: Diopsidae), two of which exhibit
             female-biased sex ratios, for the presence of these
             microbes. Type A Wolbachia was detected in four diopsid
             species, three from the genus Sphyracephala, none of which
             exhibit biased progeny sex ratios. The reproductive effects
             of the microbe were examined in one of those species, S.
             beccarii, by conducting reciprocal crosses between infected
             and uninfected strains. In this species, Wolbachia do not
             cause detectable cytoplasmic incompatibility or reduce host
             fecundity. In contrast, our results are consistent with an
             association between the microbes and enhanced male
             fertility. Possible explanations for the pattern of
             distribution and effects on male fertility include a
             predisposition for acquiring Type A Wolbachia by these flies
             and accommodation by the host genome to bacterial
             presence.},
   Doi = {10.1038/sj.hdy.6883640},
   Key = {fds252006}
}


%% Chapters in Books   
@misc{fds251945,
   Author = {Faig, KE and Nikolova, YS and Hariri, AR},
   Title = {Genetic Neuroimaging of Social Perception},
   Volume = {3},
   Pages = {97-105},
   Booktitle = {Brain Mapping: An Encyclopedic Reference},
   Year = {2015},
   Month = {February},
   ISBN = {9780123970251},
   url = {http://dx.doi.org/10.1016/B978-0-12-397025-1.00161-5},
   Doi = {10.1016/B978-0-12-397025-1.00161-5},
   Key = {fds251945}
}


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