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Publications of Maxwell Elliott    :chronological  alphabetical  by type listing:

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@article{fds357566,
   Author = {Elliott, ML and Knodt, AR and Hariri, AR},
   Title = {Striving toward translation: strategies for reliable fMRI
             measurement.},
   Journal = {Trends in Cognitive Sciences},
   Volume = {25},
   Number = {9},
   Pages = {776-787},
   Year = {2021},
   Month = {September},
   url = {http://dx.doi.org/10.1016/j.tics.2021.05.008},
   Abstract = {fMRI has considerable potential as a translational tool for
             understanding risk, prioritizing interventions, and
             improving the treatment of brain disorders. However, recent
             studies have found that many of the most widely used fMRI
             measures have low reliability, undermining this potential.
             Here, we argue that many fMRI measures are unreliable
             because they were designed to identify group effects, not to
             precisely quantify individual differences. We then highlight
             four emerging strategies [extended aggregation, reliability
             modeling, multi-echo fMRI (ME-fMRI), and stimulus design]
             that build on established psychometric properties to
             generate more precise and reliable fMRI measures. By
             adopting such strategies to improve reliability, we are
             optimistic that fMRI can fulfill its potential as a clinical
             tool.},
   Doi = {10.1016/j.tics.2021.05.008},
   Key = {fds357566}
}

@article{fds350913,
   Author = {Elliott, ML and Belsky, DW and Knodt, AR and Ireland, D and Melzer, TR and Poulton, R and Ramrakha, S and Caspi, A and Moffitt, TE and Hariri,
             AR},
   Title = {Brain-age in midlife is associated with accelerated
             biological aging and cognitive decline in a longitudinal
             birth cohort.},
   Journal = {Molecular Psychiatry},
   Volume = {26},
   Number = {8},
   Pages = {3829-3838},
   Year = {2021},
   Month = {August},
   url = {http://dx.doi.org/10.1038/s41380-019-0626-7},
   Abstract = {An individual's brainAGE is the difference between
             chronological age and age predicted from machine-learning
             models of brain-imaging data. BrainAGE has been proposed as
             a biomarker of age-related deterioration of the brain.
             Having an older brainAGE has been linked to Alzheimer's,
             dementia, and mortality. However, these findings are largely
             based on cross-sectional associations which can confuse age
             differences with cohort differences. To illuminate the
             validity of brainAGE as a biomarker of accelerated brain
             aging, a study is needed of a large cohort all born in the
             same year who nevertheless vary on brainAGE. In the Dunedin
             Study, a population-representative 1972-73 birth cohort, we
             measured brainAGE at age 45 years, as well as the pace of
             biological aging and cognitive decline in longitudinal data
             from childhood to midlife (N = 869). In this cohort, all
             chronological age 45 years, brainAGE was measured reliably
             (ICC = 0.81) and ranged from 24 to 72 years. Those with
             older midlife brainAGEs tended to have poorer cognitive
             function in both adulthood and childhood, as well as
             impaired brain health at age 3. Furthermore, those with
             older brainAGEs had an accelerated pace of biological aging,
             older facial appearance, and early signs of cognitive
             decline from childhood to midlife. These findings help to
             validate brainAGE as a potential surrogate biomarker for
             midlife intervention studies that seek to measure
             dementia-prevention efforts in midlife. However, the
             findings also caution against the assumption that brainAGE
             scores represent only age-related deterioration of the brain
             as they may also index central nervous system variation
             present since childhood.},
   Doi = {10.1038/s41380-019-0626-7},
   Key = {fds350913}
}

@article{fds356133,
   Author = {Gehred, MZ and Knodt, AR and Ambler, A and Bourassa, KJ and Danese, A and Elliott, ML and Hogan, S and Ireland, D and Poulton, R and Ramrakha, S and Reuben, A and Sison, ML and Moffitt, TE and Hariri, AR and Caspi,
             A},
   Title = {Long-term Neural Embedding of Childhood Adversity in a
             Population-Representative Birth Cohort Followed for 5
             Decades.},
   Journal = {Biological Psychiatry},
   Volume = {90},
   Number = {3},
   Pages = {182-193},
   Year = {2021},
   Month = {August},
   url = {http://dx.doi.org/10.1016/j.biopsych.2021.02.971},
   Abstract = {<h4>Background</h4>Childhood adversity has been previously
             associated with alterations in brain structure, but
             heterogeneous designs, methods, and measures have
             contributed to mixed results and have impeded progress in
             mapping the biological embedding of childhood adversity. We
             sought to identify long-term differences in structural brain
             integrity associated with childhood adversity.<h4>Methods</h4>Multiple
             regression was used to test associations between
             prospectively ascertained adversity during childhood and
             adversity retrospectively reported in adulthood with
             structural magnetic resonance imaging measures of midlife
             global and regional cortical thickness, cortical surface
             area, and subcortical gray matter volume in 861 (425 female)
             members of the Dunedin Study, a longitudinal investigation
             of a population-representative birth cohort.<h4>Results</h4>Both
             prospectively ascertained childhood adversity and
             retrospectively reported adversity were associated with
             alterations in midlife structural brain integrity, but
             associations with prospectively ascertained childhood
             adversity were consistently stronger and more widely
             distributed than associations with retrospectively reported
             childhood adversity. Sensitivity analyses revealed that
             these associations were not driven by any particular
             adversity or category of adversity (i.e., threat or
             deprivation) or by childhood socioeconomic disadvantage.
             Network enrichment analyses revealed that these associations
             were not localized but were broadly distributed along a
             hierarchical cortical gradient of information
             processing.<h4>Conclusions</h4>Exposure to childhood
             adversity broadly is associated with widespread differences
             in midlife gray matter across cortical and subcortical
             structures, suggesting that biological embedding of
             childhood adversity in the brain is long lasting, but not
             localized. Research using retrospectively reported adversity
             likely underestimates the magnitude of these associations.
             These findings may inform future research investigating
             mechanisms through which adversity becomes embedded in the
             brain and influences mental health and cognition.},
   Doi = {10.1016/j.biopsych.2021.02.971},
   Key = {fds356133}
}

@article{fds355447,
   Author = {Elliott, ML and Knodt, AR and Caspi, A and Moffitt, TE and Hariri,
             AR},
   Title = {Need for Psychometric Theory in Neuroscience Research and
             Training: Reply to Kragel et al. (2021).},
   Journal = {Psychological Science},
   Volume = {32},
   Number = {4},
   Pages = {627-629},
   Year = {2021},
   Month = {April},
   url = {http://dx.doi.org/10.1177/0956797621996665},
   Doi = {10.1177/0956797621996665},
   Key = {fds355447}
}

@article{fds355829,
   Author = {Elliott, ML and Caspi, A and Houts, RM and Ambler, A and Broadbent, JM and Hancox, RJ and Harrington, H and Hogan, S and Keenan, R and Knodt, A and Leung, JH and Melzer, TR and Purdy, SC and Ramrakha, S and Richmond-Rakerd, LS and Righarts, A and Sugden, K and Thomson, WM and Thorne, PR and Williams, BS and Wilson, G and Hariri, AR and Poulton, R and Moffitt, TE},
   Title = {Disparities in the pace of biological aging among midlife
             adults of the same chronological age have implications for
             future frailty risk and policy.},
   Journal = {Nature Aging},
   Volume = {1},
   Number = {3},
   Pages = {295-308},
   Year = {2021},
   Month = {March},
   url = {http://dx.doi.org/10.1038/s43587-021-00044-4},
   Abstract = {Some humans age faster than others. Variation in biological
             aging can be measured in midlife, but the implications of
             this variation are poorly understood. We tested associations
             between midlife biological aging and indicators of future
             frailty-risk in the Dunedin cohort of 1037 infants born the
             same year and followed to age 45. Participants' Pace of
             Aging was quantified by tracking declining function in 19
             biomarkers indexing the cardiovascular, metabolic, renal,
             immune, dental, and pulmonary systems across ages 26, 32,
             38, and 45 years. At age 45 in 2019, participants with
             faster Pace of Aging had more cognitive difficulties, signs
             of advanced brain aging, diminished sensory-motor functions,
             older appearance, and more pessimistic perceptions of aging.
             People who are aging more rapidly than same-age peers in
             midlife may prematurely need supports to sustain
             independence that are usually reserved for older adults.
             Chronological age does not adequately identify need for such
             supports.},
   Doi = {10.1038/s43587-021-00044-4},
   Key = {fds355829}
}

@article{fds355563,
   Author = {Romer, AL and Elliott, ML and Knodt, AR and Sison, ML and Ireland, D and Houts, R and Ramrakha, S and Poulton, R and Keenan, R and Melzer, TR and Moffitt, TE and Caspi, A and Hariri, AR},
   Title = {Pervasively Thinner Neocortex as a Transdiagnostic Feature
             of General Psychopathology.},
   Journal = {The American Journal of Psychiatry},
   Volume = {178},
   Number = {2},
   Pages = {174-182},
   Year = {2021},
   Month = {February},
   url = {http://dx.doi.org/10.1176/appi.ajp.2020.19090934},
   Abstract = {<h4>Objective</h4>Neuroimaging research has revealed that
             structural brain alterations are common across broad
             diagnostic families of disorders rather than specific to a
             single psychiatric disorder. Such overlap in the structural
             brain correlates of mental disorders mirrors already
             well-documented phenotypic comorbidity of psychiatric
             symptoms and diagnoses, which can be indexed by a general
             psychopathology or <i>p</i> factor. The authors hypothesized
             that if general psychopathology drives the convergence of
             structural alterations common across disorders, then 1)
             there should be few associations unique to any one
             diagnostic family of disorders, and 2) associations with the
             <i>p</i> factor should overlap with those for the broader
             diagnostic families.<h4>Methods</h4>Analyses were conducted
             on structural MRI and psychopathology data collected from
             861 members of the population-representative Dunedin
             Multidisciplinary Health and Development Study at age
             45.<h4>Results</h4>Study members with high scores across
             three broad diagnostic families of disorders (externalizing,
             internalizing, thought disorder) exhibited highly
             overlapping patterns of reduced global and widely
             distributed parcel-wise neocortical thickness. Study members
             with high <i>p</i> factor scores exhibited patterns of
             reduced global and parcel-wise neocortical thickness nearly
             identical to those associated with the three broad
             diagnostic families.<h4>Conclusions</h4>A pattern of
             pervasively reduced neocortical thickness appears to be
             common across all forms of mental disorders and may
             represent a transdiagnostic feature of general
             psychopathology. As has been documented with regard to
             symptoms and diagnoses, the underlying brain structural
             correlates of mental disorders may not exhibit specificity,
             and the continued pursuit of such specific correlates may
             limit progress toward more effective strategies for
             etiological understanding, prevention, and
             intervention.},
   Doi = {10.1176/appi.ajp.2020.19090934},
   Key = {fds355563}
}

@article{fds358354,
   Author = {Kim, MJ and Elliott, ML and Knodt, AR and Hariri,
             AR},
   Title = {A Connectome-Wide Functional Signature of Trait
             Anger},
   Journal = {Clinical Psychological Science : a Journal of the
             Association for Psychological Science},
   Year = {2021},
   Month = {January},
   url = {http://dx.doi.org/10.1177/21677026211030240},
   Abstract = {Past research on the brain correlates of trait anger has
             been limited by small sample sizes, a focus on relatively
             few regions of interest, and poor test–retest reliability
             of functional brain measures. To address these limitations,
             we conducted a data-driven analysis of variability in
             connectome-wide functional connectivity in a sample of 1,048
             young adult volunteers. Multidimensional matrix regression
             analysis showed that self-reported trait anger maps onto
             variability in the whole-brain functional connectivity
             patterns of three brain regions that serve action-related
             functions: bilateral supplementary motor areas and the right
             lateral frontal pole. We then demonstrate that trait anger
             modulates the functional connectivity of these regions with
             canonical brain networks supporting somatomotor, affective,
             self-referential, and visual information processes. Our
             findings offer novel neuroimaging evidence for interpreting
             trait anger as a greater propensity to provoked action,
             which supports ongoing efforts to understand its utility as
             a potential transdiagnostic marker for disordered states
             characterized by aggressive behavior.},
   Doi = {10.1177/21677026211030240},
   Key = {fds358354}
}

@article{fds351245,
   Author = {Rasmussen, LJH and Caspi, A and Ambler, A and Danese, A and Elliott, M and Eugen-Olsen, J and Hariri, AR and Harrington, H and Houts, R and Poulton, R and Ramrakha, S and Sugden, K and Williams, B and Moffitt,
             TE},
   Title = {Association Between Elevated suPAR, a New Biomarker of
             Inflammation, and Accelerated Aging.},
   Journal = {The Journals of Gerontology. Series A, Biological Sciences
             and Medical Sciences},
   Volume = {76},
   Number = {2},
   Pages = {318-327},
   Year = {2021},
   Month = {January},
   url = {http://dx.doi.org/10.1093/gerona/glaa178},
   Abstract = {<h4>Background</h4>To understand and measure the association
             between chronic inflammation, aging, and age-related
             diseases, broadly applicable standard biomarkers of systemic
             chronic inflammation are needed. We tested whether elevated
             blood levels of the emerging chronic inflammation marker
             soluble urokinase plasminogen activator receptor (suPAR)
             were associated with accelerated aging, lower functional
             capacity, and cognitive decline.<h4>Methods</h4>We used data
             from the Dunedin Study, a population-representative
             1972-1973 New Zealand birth cohort (n = 1037) that has
             observed participants to age 45 years. Plasma suPAR levels
             were analyzed at ages 38 and 45 years. We performed
             regression analyses adjusted for sex, smoking, C-reactive
             protein, and current health conditions.<h4>Results</h4>Of
             997 still-living participants, 875 (88%) had plasma suPAR
             measured at age 45. Elevated suPAR was associated with
             accelerated pace of biological aging across multiple organ
             systems, older facial appearance, and with structural signs
             of older brain age. Moreover, participants with higher suPAR
             levels had greater decline in physical function and
             cognitive function from childhood to adulthood compared to
             those with lower suPAR levels. Finally, improvements in
             health habits between ages 38 and 45 (smoking cessation or
             increased physical activity) were associated with less steep
             increases in suPAR levels over those years.<h4>Conclusions</h4>Our
             findings provide initial support for the utility of suPAR in
             studying the role of chronic inflammation in accelerated
             aging and functional decline.},
   Doi = {10.1093/gerona/glaa178},
   Key = {fds351245}
}

@article{fds354592,
   Author = {Richmond-Rakerd, LS and Caspi, A and Ambler, A and d'Arbeloff, T and de
             Bruine, M and Elliott, M and Harrington, H and Hogan, S and Houts, RM and Ireland, D and Keenan, R and Knodt, AR and Melzer, TR and Park, S and Poulton, R and Ramrakha, S and Rasmussen, LJH and Sack, E and Schmidt,
             AT and Sison, ML and Wertz, J and Hariri, AR and Moffitt,
             TE},
   Title = {Childhood self-control forecasts the pace of midlife aging
             and preparedness for old age.},
   Journal = {Proceedings of the National Academy of Sciences of the
             United States of America},
   Volume = {118},
   Number = {3},
   Pages = {e2010211118},
   Year = {2021},
   Month = {January},
   url = {http://dx.doi.org/10.1073/pnas.2010211118},
   Abstract = {The ability to control one's own emotions, thoughts, and
             behaviors in early life predicts a range of positive
             outcomes in later life, including longevity. Does it also
             predict how well people age? We studied the association
             between self-control and midlife aging in a
             population-representative cohort of children followed from
             birth to age 45 y, the Dunedin Study. We measured children's
             self-control across their first decade of life using a
             multi-occasion/multi-informant strategy. We measured their
             pace of aging and aging preparedness in midlife using
             measures derived from biological and physiological
             assessments, structural brain-imaging scans, observer
             ratings, self-reports, informant reports, and administrative
             records. As adults, children with better self-control aged
             more slowly in their bodies and showed fewer signs of aging
             in their brains. By midlife, these children were also better
             equipped to manage a range of later-life health, financial,
             and social demands. Associations with children's
             self-control could be separated from their social class
             origins and intelligence, indicating that self-control might
             be an active ingredient in healthy aging. Children also
             shifted naturally in their level of self-control across
             adult life, suggesting the possibility that self-control may
             be a malleable target for intervention. Furthermore,
             individuals' self-control in adulthood was associated with
             their aging outcomes after accounting for their self-control
             in childhood, indicating that midlife might offer another
             window of opportunity to promote healthy
             aging.},
   Doi = {10.1073/pnas.2010211118},
   Key = {fds354592}
}

@article{fds356036,
   Author = {d'Arbeloff, T and Elliott, ML and Knodt, AR and Sison, M and Melzer, TR and Ireland, D and Ramrakha, S and Poulton, R and Caspi, A and Moffitt, TE and Hariri, AR},
   Title = {Midlife Cardiovascular Fitness Is Reflected in the Brain's
             White Matter.},
   Journal = {Frontiers in Aging Neuroscience},
   Volume = {13},
   Pages = {652575},
   Year = {2021},
   Month = {January},
   url = {http://dx.doi.org/10.3389/fnagi.2021.652575},
   Abstract = {Disappointing results from clinical trials designed to delay
             structural brain decline and the accompanying increase in
             risk for dementia in older adults have precipitated a shift
             in testing promising interventions from late in life toward
             midlife before irreversible damage has accumulated. This
             shift, however, requires targeting midlife biomarkers that
             are associated with clinical changes manifesting only in
             late life. Here we explored possible links between one
             putative biomarker, distributed integrity of brain white
             matter, and two intervention targets, cardiovascular fitness
             and healthy lifestyle behaviors, in midlife. At age 45,
             fractional anisotropy (FA) derived from diffusion weighted
             MRI was used to estimate the microstructural integrity of
             distributed white matter tracts in a population-representative
             birth cohort. Age-45 cardiovascular fitness
             (VO<sub>2</sub>Max; <i>N</i> = 801) was estimated from heart
             rates obtained during submaximal exercise tests; age-45
             healthy lifestyle behaviors were estimated using the Nyberg
             Health Index (<i>N</i> = 854). Ten-fold cross-validated
             elastic net predictive modeling revealed that estimated
             VO<sub>2</sub>Max was modestly associated with distributed
             FA. In contrast, there was no significant association
             between Nyberg Health Index scores and FA. Our findings
             suggest that cardiovascular fitness levels, but not healthy
             lifestyle behaviors, are associated with the distributed
             integrity of white matter in the brain in midlife. These
             patterns could help inform future clinical intervention
             research targeting ADRDs.},
   Doi = {10.3389/fnagi.2021.652575},
   Key = {fds356036}
}

@article{fds353274,
   Author = {Reuben, A and Elliott, ML and Abraham, WC and Broadbent, J and Houts,
             RM and Ireland, D and Knodt, AR and Poulton, R and Ramrakha, S and Hariri,
             AR and Caspi, A and Moffitt, TE},
   Title = {Association of Childhood Lead Exposure With MRI Measurements
             of Structural Brain Integrity in Midlife.},
   Journal = {Jama},
   Volume = {324},
   Number = {19},
   Pages = {1970-1979},
   Year = {2020},
   Month = {November},
   url = {http://dx.doi.org/10.1001/jama.2020.19998},
   Abstract = {<h4>Importance</h4>Childhood lead exposure has been linked
             to disrupted brain development, but long-term consequences
             for structural brain integrity are unknown.<h4>Objective</h4>To
             test the hypothesis that childhood lead exposure is
             associated with magnetic resonance imaging (MRI)
             measurements of lower structural integrity of the brain in
             midlife.<h4>Design, setting, and participants</h4>The
             Dunedin Study followed a population-representative 1972-1973
             birth cohort in New Zealand (N = 564 analytic sample) to
             age 45 years (until April 2019).<h4>Exposures</h4>Childhood
             blood lead levels measured at age 11 years.<h4>Main outcomes
             and measures</h4>Structural brain integrity at age 45 years
             assessed via MRI (primary outcomes): gray matter (cortical
             thickness, surface area, hippocampal volume), white matter
             (white matter hyperintensities, fractional anisotropy
             [theoretical range, 0 {diffusion is perfectly isotropic} to
             100 {diffusion is perfectly anisotropic}]), and the Brain
             Age Gap Estimation (BrainAGE), a composite index of the gap
             between chronological age and a machine learning
             algorithm-estimated brain age (0 indicates a brain age
             equivalent to chronological age; positive and negative
             values represent an older and younger brain age,
             respectively). Cognitive function at age 45 years was
             assessed objectively via the Wechsler Adult Intelligence
             Scale IV (IQ range, 40-160, standardized to a mean of 100
             [SD, 15]) and subjectively via informant and self-reports
             (z-score units; scale mean, 0 [SD, 1]).<h4>Results</h4>Of
             1037 original participants, 997 were alive at age 45 years,
             of whom 564 (57%) had received lead testing at age 11 years
             (302 [54%] male) (median follow-up, 34 [interquartile range,
             33.7-34.7] years). Mean blood lead level at age 11 years was
             10.99 (SD, 4.63) μg/dL. After adjusting for covariates,
             each 5-μg/dL higher childhood blood lead level was
             significantly associated with 1.19-cm2 smaller cortical
             surface area (95% CI, -2.35 to -0.02 cm2; P = .05),
             0.10-cm3 smaller hippocampal volume (95% CI, -0.17 to -0.03
             cm3; P = .006), lower global fractional anisotropy
             (b = -0.12; 95% CI, -0.24 to -0.01; P = .04), and a
             BrainAGE index 0.77 years older (95% CI, 0.02-1.51 years;
             P = .05) at age 45 years. There were no statistically
             significant associations between blood lead level and
             log-transformed white matter hyperintensity volume
             (b = 0.05 log mm3; 95% CI, -0.02 to 0.13 log mm3;
             P = .17) or mean cortical thickness (b = -0.004 mm;
             95% CI, -0.012 to 0.004 mm; P = .39). Each 5-μg/dL
             higher childhood blood lead level was significantly
             associated with a 2.07-point lower IQ score at age 45 years
             (95% CI, -3.39 to -0.74; P = .002) and a 0.12-point
             higher score on informant-rated cognitive problems (95% CI,
             0.01-0.23; P = .03). There was no statistically
             significant association between childhood blood lead levels
             and self-reported cognitive problems (b = -0.02 points;
             95% CI, -0.10 to 0.07; P = .68).<h4>Conclusions and
             relevance</h4>In this longitudinal cohort study with a
             median 34-year follow-up, higher childhood blood lead level
             was associated with differences in some MRI measures of
             brain structure that suggested lower structural brain
             integrity in midlife. Because of the large number of
             statistical comparisons, some findings may represent type I
             error.},
   Doi = {10.1001/jama.2020.19998},
   Key = {fds353274}
}

@article{fds350908,
   Author = {Elliott, ML},
   Title = {MRI-based biomarkers of accelerated aging and dementia risk
             in midlife: how close are we?},
   Journal = {Ageing Research Reviews},
   Volume = {61},
   Pages = {101075},
   Year = {2020},
   Month = {August},
   url = {http://dx.doi.org/10.1016/j.arr.2020.101075},
   Abstract = {The global population is aging, leading to an increasing
             burden of age-related neurodegenerative disease. Efforts to
             intervene against age-related dementias in older adults have
             generally proven ineffective. These failures suggest that a
             lifetime of brain aging may be difficult to reverse once
             widespread deterioration has occurred. To test interventions
             in younger populations, biomarkers of brain aging are needed
             that index subtle signs of accelerated brain deterioration
             that are part of the putative pathway to dementia. Here I
             review potential MRI-based biomarkers that could connect
             midlife brain aging to later life dementia. I survey the
             literature with three questions in mind, 1) Does the
             biomarker index age-related changes across the lifespan? 2)
             Does the biomarker index cognitive ability and cognitive
             decline? 3) Is the biomarker sensitive to known risk factors
             for dementia? I find that while there is preliminary support
             for some midlife MRI-based biomarkers for accelerated aging,
             the longitudinal research that would best answer these
             questions is still in its infancy and needs to be further
             developed. I conclude with suggestions for future
             research.},
   Doi = {10.1016/j.arr.2020.101075},
   Key = {fds350908}
}

@article{fds350909,
   Author = {Elliott, ML and Knodt, AR and Ireland, D and Morris, ML and Poulton, R and Ramrakha, S and Sison, ML and Moffitt, TE and Caspi, A and Hariri,
             AR},
   Title = {What Is the Test-Retest Reliability of Common
             Task-Functional MRI Measures? New Empirical Evidence and a
             Meta-Analysis.},
   Journal = {Psychological Science},
   Volume = {31},
   Number = {7},
   Pages = {792-806},
   Year = {2020},
   Month = {July},
   url = {http://dx.doi.org/10.1177/0956797620916786},
   Abstract = {Identifying brain biomarkers of disease risk is a growing
             priority in neuroscience. The ability to identify meaningful
             biomarkers is limited by measurement reliability; unreliable
             measures are unsuitable for predicting clinical outcomes.
             Measuring brain activity using task functional MRI (fMRI) is
             a major focus of biomarker development; however, the
             reliability of task fMRI has not been systematically
             evaluated. We present converging evidence demonstrating poor
             reliability of task-fMRI measures. First, a meta-analysis of
             90 experiments (<i>N</i> = 1,008) revealed poor overall
             reliability-mean intraclass correlation coefficient (ICC) =
             .397. Second, the test-retest reliabilities of activity in a
             priori regions of interest across 11 common fMRI tasks
             collected by the Human Connectome Project (<i>N</i> = 45)
             and the Dunedin Study (<i>N</i> = 20) were poor (ICCs =
             .067-.485). Collectively, these findings demonstrate that
             common task-fMRI measures are not currently suitable for
             brain biomarker discovery or for individual-differences
             research. We review how this state of affairs came to be and
             highlight avenues for improving task-fMRI
             reliability.},
   Doi = {10.1177/0956797620916786},
   Key = {fds350909}
}

@article{fds350910,
   Author = {Caspi, A and Houts, RM and Ambler, A and Danese, A and Elliott, ML and Hariri, A and Harrington, H and Hogan, S and Poulton, R and Ramrakha, S and Rasmussen, LJH and Reuben, A and Richmond-Rakerd, L and Sugden, K and Wertz, J and Williams, BS and Moffitt, TE},
   Title = {Longitudinal Assessment of Mental Health Disorders and
             Comorbidities Across 4 Decades Among Participants in the
             Dunedin Birth Cohort Study.},
   Journal = {Jama Network Open},
   Volume = {3},
   Number = {4},
   Pages = {e203221},
   Year = {2020},
   Month = {April},
   url = {http://dx.doi.org/10.1001/jamanetworkopen.2020.3221},
   Abstract = {<h4>Importance</h4>Mental health professionals typically
             encounter patients at 1 point in patients' lives. This
             cross-sectional window understandably fosters focus on the
             current presenting diagnosis. Research programs, treatment
             protocols, specialist clinics, and specialist journals are
             oriented to presenting diagnoses, on the assumption that
             diagnosis informs about causes and prognosis. This study
             tests an alternative hypothesis: people with mental
             disorders experience many different kinds of disorders
             across diagnostic families, when followed for 4
             decades.<h4>Objective</h4>To describe mental disorder life
             histories across the first half of the life
             course.<h4>Design, setting, and participants</h4>This cohort
             study involved participants born in New Zealand from 1972 to
             1973 who were enrolled in the population-representative
             Dunedin Study. Participants were observed from birth to age
             45 years (until April 2019). Data were analyzed from May
             2019 to January 2020.<h4>Main outcomes and
             measures</h4>Diagnosed impairing disorders were assessed 9
             times from ages 11 to 45 years. Brain function was assessed
             through neurocognitive examinations conducted at age 3
             years, neuropsychological testing during childhood and
             adulthood, and midlife neuroimaging-based brain
             age.<h4>Results</h4>Of 1037 original participants (535 male
             [51.6%]), 1013 had mental health data available. The
             proportions of participants meeting the criteria for a
             mental disorder were as follows: 35% (346 of 975) at ages 11
             to 15 years, 50% (473 of 941) at age 18 years, 51% (489 of
             961) at age 21 years, 48% (472 of 977) at age 26 years, 46%
             (444 of 969) at age 32 years, 45% (429 of 955) at age 38
             years, and 44% (407 of 927) at age 45 years. The onset of
             the disorder occurred by adolescence for 59% of participants
             (600 of 1013), eventually affecting 86% of the cohort (869
             of 1013) by midlife. By age 45 years, 85% of participants
             (737 of 869) with a disorder had accumulated comorbid
             diagnoses. Participants with adolescent-onset disorders
             subsequently presented with disorders at more past-year
             assessments (r = 0.71; 95% CI, 0.68 to 0.74;
             P < .001) and met the criteria for more diverse
             disorders (r = 0.64; 95% CI, 0.60 to 0.67;
             P < .001). Confirmatory factor analysis summarizing
             mental disorder life histories across 4 decades identified a
             general factor of psychopathology, the p-factor.
             Longitudinal analyses showed that high p-factor scores
             (indicating extensive mental disorder life histories) were
             antedated by poor neurocognitive functioning at age 3 years
             (r = -0.18; 95% CI, -0.24 to -0.12; P < .001), were
             accompanied by childhood-to-adulthood cognitive decline
             (r = -0.11; 95% CI, -0.17 to -0.04; P < .001), and
             were associated with older brain age at midlife
             (r = 0.14; 95% CI, 0.07 to 0.20; P < .001).<h4>Conclusions
             and relevance</h4>These findings suggest that mental
             disorder life histories shift among different successive
             disorders. Data from the present study, alongside nationwide
             data from Danish health registers, inform a life-course
             perspective on mental disorders. This perspective cautions
             against overreliance on diagnosis-specific research and
             clinical protocols.},
   Doi = {10.1001/jamanetworkopen.2020.3221},
   Key = {fds350910}
}

@article{fds350911,
   Author = {Burr, DA and d'Arbeloff, T and Elliott, ML and Knodt, AR and Brigidi,
             BD and Hariri, AR},
   Title = {Functional connectivity predicts the dispositional use of
             expressive suppression but not cognitive
             reappraisal.},
   Journal = {Brain and Behavior},
   Volume = {10},
   Number = {2},
   Pages = {e01493},
   Year = {2020},
   Month = {February},
   url = {http://dx.doi.org/10.1002/brb3.1493},
   Abstract = {<h4>Introduction</h4>Previous research has identified
             specific brain regions associated with regulating emotion
             using common strategies such as expressive suppression and
             cognitive reappraisal. However, most research focuses on a
             priori regions and directs participants how to regulate,
             which may not reflect how people naturally regulate outside
             the laboratory.<h4>Method</h4>Here, we used a data-driven
             approach to investigate how individual differences in
             distributed intrinsic functional brain connectivity predict
             emotion regulation tendency outside the laboratory.
             Specifically, we used connectome-based predictive modeling
             to extract functional connections in the brain significantly
             related to the dispositional use of suppression and
             reappraisal. These edges were then used in a predictive
             model and cross-validated in novel participants to identify
             a neural signature that reflects individual differences in
             the tendency to suppress and reappraise emotion.<h4>Results</h4>We
             found a significant neural signature for the dispositional
             use of suppression, but not reappraisal. Within this
             whole-brain signature, the intrinsic connectivity of the
             default mode network was most informative of suppression
             tendency. In addition, the predictive performance of this
             model was significant in males, but not females.<h4>Conclusion</h4>These
             findings help inform how whole-brain networks of functional
             connectivity characterize how people tend to regulate
             emotion outside the laboratory.},
   Doi = {10.1002/brb3.1493},
   Key = {fds350911}
}

@article{fds350912,
   Author = {Reuben, A and Elliott, M and Caspi, A},
   Title = {Implications of legacy lead for children's brain
             development.},
   Journal = {Nature Medicine},
   Volume = {26},
   Number = {1},
   Pages = {23-25},
   Year = {2020},
   Month = {January},
   url = {http://dx.doi.org/10.1038/s41591-019-0731-9},
   Doi = {10.1038/s41591-019-0731-9},
   Key = {fds350912}
}

@article{fds350914,
   Author = {Gregory, MD and Mervis, CB and Elliott, ML and Kippenhan, JS and Nash,
             T and B Czarapata and J and Prabhakaran, R and Roe, K and Eisenberg, DP and Kohn, PD and Berman, KF},
   Title = {Williams syndrome hemideletion and LIMK1 variation both
             affect dorsal stream functional connectivity.},
   Journal = {Brain},
   Volume = {142},
   Number = {12},
   Pages = {3963-3974},
   Year = {2019},
   Month = {December},
   url = {http://dx.doi.org/10.1093/brain/awz323},
   Abstract = {Williams syndrome is a rare genetic disorder caused by
             hemizygous deletion of ∼1.6 Mb affecting 26 genes on
             chromosome 7 (7q11.23) and is clinically typified by two
             cognitive/behavioural hallmarks: marked visuospatial
             deficits relative to verbal and non-verbal reasoning
             abilities and hypersocial personality. Clear knowledge of
             the circumscribed set of genes that are affected in Williams
             syndrome, along with the well-characterized neurobehavioural
             phenotype, offers the potential to elucidate neurogenetic
             principles that may apply in genetically and clinically more
             complex settings. The intraparietal sulcus, in the dorsal
             visual processing stream, has been shown to be structurally
             and functionally altered in Williams syndrome, providing a
             target for investigating resting-state functional
             connectivity and effects of specific genes hemideleted in
             Williams syndrome. Here, we tested for effects of the LIMK1
             gene, deleted in Williams syndrome and important for
             neuronal maturation and migration, on intraparietal sulcus
             functional connectivity. We first defined a target brain
             phenotype by comparing intraparietal sulcus resting
             functional connectivity in individuals with Williams
             syndrome, in whom LIMK1 is hemideleted, with typically
             developing children. Then in two separate cohorts from the
             general population, we asked whether intraparietal sulcus
             functional connectivity patterns similar to those found in
             Williams syndrome were associated with sequence variation of
             the LIMK1 gene. Four independent between-group comparisons
             of resting-state functional MRI data (total n = 510) were
             performed: (i) 20 children with Williams syndrome compared
             to 20 age- and sex-matched typically developing children;
             (ii) a discovery cohort of 99 healthy adults stratified by
             LIMK1 haplotype; (iii) a replication cohort of 32 healthy
             adults also stratified by LIMK1 haplotype; and (iv) 339
             healthy adolescent children stratified by LIMK1 haplotype.
             For between-group analyses, differences in intraparietal
             sulcus resting-state functional connectivity were calculated
             comparing children with Williams syndrome to matched
             typically developing children and comparing LIMK1 haplotype
             groups in each of the three general population cohorts
             separately. Consistent with the visuospatial construction
             impairment and hypersocial personality that typify Williams
             syndrome, the Williams syndrome cohort exhibited opposite
             patterns of intraparietal sulcus functional connectivity
             with visual processing regions and social processing
             regions: decreased circuit function in the former and
             increased circuit function in the latter. All three general
             population groups also showed LIMK1 haplotype-related
             differences in intraparietal sulcus functional connectivity
             localized to the fusiform gyrus, a visual processing region
             also identified in the Williams syndrome-typically
             developing comparison. These results suggest a neurogenetic
             mechanism, in part involving LIMK1, that may bias neural
             circuit function in both the general population and
             individuals with Williams syndrome.},
   Doi = {10.1093/brain/awz323},
   Key = {fds350914}
}

@article{fds350915,
   Author = {Rasmussen, LJH and Caspi, A and Ambler, A and Broadbent, JM and Cohen,
             HJ and d'Arbeloff, T and Elliott, M and Hancox, RJ and Harrington, H and Hogan, S and Houts, R and Ireland, D and Knodt, AR and Meredith-Jones,
             K and Morey, MC and Morrison, L and Poulton, R and Ramrakha, S and Richmond-Rakerd, L and Sison, ML and Sneddon, K and Thomson, WM and Hariri, AR and Moffitt, TE},
   Title = {Association of Neurocognitive and Physical Function With
             Gait Speed in Midlife.},
   Journal = {Jama Network Open},
   Volume = {2},
   Number = {10},
   Pages = {e1913123},
   Year = {2019},
   Month = {October},
   url = {http://dx.doi.org/10.1001/jamanetworkopen.2019.13123},
   Abstract = {Importance: Gait speed is a well-known indicator of risk of
             functional decline and mortality in older adults, but little
             is known about the factors associated with gait speed
             earlier in life. Objectives: To test the hypothesis that
             slow gait speed reflects accelerated biological aging at
             midlife, as well as poor neurocognitive functioning in
             childhood and cognitive decline from childhood to midlife.
             Design, Setting, and Participants: This cohort study uses
             data from the Dunedin Multidisciplinary Health and
             Development Study, a population-based study of a
             representative 1972 to 1973 birth cohort in New Zealand that
             observed participants to age 45 years (until April 2019).
             Data analysis was performed from April to June 2019.
             Exposures: Childhood neurocognitive functions and
             accelerated aging, brain structure, and concurrent physical
             and cognitive functions in adulthood. Main Outcomes and
             Measures: Gait speed at age 45 years, measured under 3
             walking conditions: usual, dual task, and maximum gait
             speeds. Results: Of the 1037 original participants (91% of
             eligible births; 535 [51.6%] male), 997 were alive at age 45
             years, of whom 904 (90.7%) had gait speed measured (455
             [50.3%] male; 93% white). The mean (SD) gait speeds were
             1.30 (0.17) m/s for usual gait, 1.16 (0.23) m/s for dual
             task gait, and 1.99 (0.29) m/s for maximum gait. Adults with
             more physical limitations (standardized regression
             coefficient [β], -0.27; 95% CI, -0.34 to -0.21;
             P < .001), poorer physical functions (ie, weak grip
             strength [β, 0.36; 95% CI, 0.25 to 0.46], poor balance [β,
             0.28; 95% CI, 0.21 to 0.34], poor visual-motor coordination
             [β, 0.24; 95% CI, 0.17 to 0.30], and poor performance on
             the chair-stand [β, 0.34; 95% CI, 0.27 to 0.40] or 2-minute
             step tests [β, 0.33; 95% CI, 0.27 to 0.39]; all
             P < .001), accelerated biological aging across multiple
             organ systems (β, -0.33; 95% CI, -0.40 to -0.27;
             P < .001), older facial appearance (β, -0.25; 95% CI,
             -0.31 to -0.18; P < .001), smaller brain volume (β,
             0.15; 95% CI, 0.06 to 0.23; P < .001), more cortical
             thinning (β, 0.09; 95% CI, 0.02 to 0.16; P = .01),
             smaller cortical surface area (β, 0.13; 95% CI, 0.04 to
             0.21; P = .003), and more white matter hyperintensities
             (β, -0.09; 95% CI, -0.15 to -0.02; P = .01) had slower
             gait speed. Participants with lower IQ in midlife (β, 0.38;
             95% CI, 0.32 to 0.44; P < .001) and participants who
             exhibited cognitive decline from childhood to adulthood (β,
             0.10; 95% CI, 0.04 to 0.17; P < .001) had slower gait at
             age 45 years. Those with poor neurocognitive functioning as
             early as age 3 years had slower gait in midlife (β, 0.26;
             95% CI, 0.20 to 0.32; P < .001). Conclusions and
             Relevance: Adults' gait speed is associated with more than
             geriatric functional status; it is also associated with
             midlife aging and lifelong brain health.},
   Doi = {10.1001/jamanetworkopen.2019.13123},
   Key = {fds350915}
}

@article{fds350916,
   Author = {Romer, A and Elliott, M and Knodt, A and Sison, M and Ireland, D and Houts,
             R and Ramrakha, S and Poulton, R and Keenan, R and Melzer, T and Moffitt,
             T and Caspi, A and Hariri, A},
   Title = {Pervasively thinner neocortex as a transdiagnostic feature
             of general psychopathology},
   Year = {2019},
   Month = {September},
   url = {http://dx.doi.org/10.1101/788232},
   Abstract = {<h4>Objective</h4> Neuroimaging research has revealed that
             structural brain alterations are common across broad
             diagnostic families of disorders rather than specific to a
             single psychiatric disorder. Such overlap in the structural
             brain correlates of mental disorders mirrors already
             well-documented phenotypic comorbidity of psychiatric
             symptoms and diagnoses, which can be indexed by a general
             psychopathology or p factor. We hypothesized that if general
             psychopathology drives the convergence of structural
             alterations common across disorders then 1) there should be
             few associations unique to any one diagnostic family of
             disorders, and 2) associations with the p factor should
             overlap with those for the broader diagnostic families.
             <h4>Methods</h4> Analyses were conducted on structural MRI
             and psychopathology data collected from 861 members of the
             population representative Dunedin Study at age 45.
             <h4>Results</h4> Study members with high scores across three
             broad diagnostic families of disorders (Externalizing,
             Internalizing, Thought Disorder) exhibited highly
             overlapping patterns of reduced global and widely
             distributed parcel-wise neocortical thickness. Study members
             with high p factor scores exhibited patterns of reduced
             global and parcel-wise neocortical thickness nearly
             identical to those associated with the three broad
             diagnostic families. <h4>Conclusions</h4> A pattern of
             pervasively reduced neocortical thickness appears common
             across all forms of mental disorders and may represent a
             transdiagnostic feature of general psychopathology. As has
             been documented with regard to symptoms and diagnoses, the
             underlying brain structural correlates of mental disorders
             may not exhibit specificity, the continued pursuit of which
             may limit progress toward more effective strategies for
             etiological understanding, prevention, and
             intervention.},
   Doi = {10.1101/788232},
   Key = {fds350916}
}

@article{fds350917,
   Author = {Avinun, R and Nevo, A and Knodt, AR and Elliott, ML and Hariri,
             AR},
   Title = {A genome-wide association study-derived polygenic score for
             interleukin-1β is associated with hippocampal volume in two
             samples.},
   Journal = {Human Brain Mapping},
   Volume = {40},
   Number = {13},
   Pages = {3910-3917},
   Year = {2019},
   Month = {September},
   url = {http://dx.doi.org/10.1002/hbm.24639},
   Abstract = {Accumulating research suggests that the pro-inflammatory
             cytokine interleukin-1β (IL-1β) has a modulatory effect on
             the hippocampus, a brain structure important for learning
             and memory as well as linked with both psychiatric and
             neurodegenerative disorders. Here, we used an imaging
             genetics strategy to test an association between an IL-1β
             polygenic score and hippocampal volume in two independent
             samples. Our polygenic score was derived using summary
             statistics from a recent genome-wide association study of
             circulating cytokines that included IL-1β (N = 3,309). In
             the first sample of 512 non-Hispanic Caucasian university
             students (274 women, mean age 19.78 ± 1.24 years) from
             the Duke Neurogenetics Study, we identified a significant
             positive correlation between IL-1β polygenic scores and
             hippocampal volume. This positive association was
             successfully replicated in a second sample of 7,960 white
             British volunteers (4,158 women, mean age 62.63 ± 7.45
             years) from the UK Biobank. Our results lend further support
             in humans, to the link between IL-1β and the structure of
             the hippocampus.},
   Doi = {10.1002/hbm.24639},
   Key = {fds350917}
}

@article{fds350918,
   Author = {Elliott, M and Belsky, D and Knodt, A and Ireland, D and Melzer, T and Poulton, R and Ramrakha, S and Caspi, A and Moffitt, T and Hariri,
             A},
   Title = {Brain-age in midlife is associated with accelerated
             biological aging and cognitive decline in a longitudinal
             birth-cohort},
   Year = {2019},
   Month = {July},
   url = {http://dx.doi.org/10.1101/712851},
   Abstract = {An individual’s brain-age is the difference between
             chronological age and age predicted from machine-learning
             models of brain-imaging data. Brain-age has been proposed as
             a biomarker of age-related deterioration of the brain.
             Having an older brain-age has been linked to Alzheimer’s,
             dementia and mortality. However, these findings are largely
             based on cross-sectional associations which can confuse age
             differences with cohort differences. To illuminate the
             validity of brain-age a biomarker of accelerated brain
             aging, a study is needed of a large cohort all born the same
             year who nevertheless vary on brain-age. In a
             population-representative 1972-73 birth cohort we measured
             brain-age at age 45, as well as the pace of biological aging
             and cognitive decline in longitudinal data from childhood to
             midlife (N=869). In this cohort, all chronological age 45
             years, brain-age was measured reliably (ICC=.81) and ranged
             from 24 to 72 years. Those with older midlife brain-ages
             tended to have poorer cognitive function in both adulthood
             and childhood, as well as impaired brain health at age 3.
             Furthermore, those with older brain-ages had an accelerated
             pace of biological aging, older facial appearance and early
             signs of cognitive decline from childhood to midlife. These
             findings help to validate brain-age as a potential surrogate
             biomarker for midlife intervention studies that seek to
             measure treatment response to dementia-prevention efforts in
             midlife. However, the findings also caution against the
             assumption that brain-age scores represent only age-related
             deterioration of the brain as they may also index central
             nervous system variation present since childhood.},
   Doi = {10.1101/712851},
   Key = {fds350918}
}

@article{fds350919,
   Author = {Elliott, ML and Belsky, DW and Anderson, K and Corcoran, DL and Ge, T and Knodt, A and Prinz, JA and Sugden, K and Williams, B and Ireland, D and Poulton, R and Caspi, A and Holmes, A and Moffitt, T and Hariri,
             AR},
   Title = {A Polygenic Score for Higher Educational Attainment is
             Associated with Larger Brains.},
   Journal = {Cerebral Cortex (New York, N.Y. : 1991)},
   Volume = {29},
   Number = {8},
   Pages = {3496-3504},
   Year = {2019},
   Month = {July},
   url = {http://dx.doi.org/10.1093/cercor/bhy219},
   Abstract = {People who score higher on intelligence tests tend to have
             larger brains. Twin studies suggest the same genetic factors
             influence both brain size and intelligence. This has led to
             the hypothesis that genetics influence intelligence partly
             by contributing to the development of larger brains. We
             tested this hypothesis using four large imaging genetics
             studies (combined N = 7965) with polygenic scores derived
             from a genome-wide association study (GWAS) of educational
             attainment, a correlate of intelligence. We conducted
             meta-analysis to test associations among participants'
             genetics, total brain volume (i.e., brain size), and
             cognitive test performance. Consistent with previous
             findings, participants with higher polygenic scores achieved
             higher scores on cognitive tests, as did participants with
             larger brains. Participants with higher polygenic scores
             also had larger brains. We found some evidence that brain
             size partly mediated associations between participants'
             education polygenic scores and their cognitive test
             performance. Effect sizes were larger in the
             population-based samples than in the convenience-based
             samples. Recruitment and retention of population-representative
             samples should be a priority for neuroscience research.
             Findings suggest promise for studies integrating GWAS
             discoveries with brain imaging to understand neurobiology
             linking genetics with cognitive performance.},
   Doi = {10.1093/cercor/bhy219},
   Key = {fds350919}
}

@article{fds350920,
   Author = {Elliott, M and Knodt, A and Ireland, D and Morris, M and Poulton, R and Ramrakha, S and Sison, M and Moffitt, T and Caspi, A and Hariri,
             A},
   Title = {What is the test-retest reliability of common task-fMRI
             measures? New empirical evidence and a meta-analysis},
   Year = {2019},
   Month = {June},
   url = {http://dx.doi.org/10.1101/681700},
   Abstract = {Identifying brain biomarkers of disease risk is a growing
             priority in neuroscience. The ability to identify meaningful
             biomarkers is limited by measurement reliability; unreliable
             measures are unsuitable for predicting clinical outcomes.
             Measuring brain activity using task-fMRI is a major focus of
             biomarker development; however, the reliability of task-fMRI
             has not been systematically evaluated. We present converging
             evidence demonstrating poor reliability of task-fMRI
             measures. First, a meta-analysis of 90 experiments (N=1,008)
             revealed poor overall reliability (mean ICC=.397). Second,
             the test-retest reliabilities of activity in a priori
             regions of interest across 11 common fMRI tasks collected in
             the context of the Human Connectome Project (N=45) and the
             Dunedin Study (N=20) were poor (ICCs=.067-.485).
             Collectively, these findings demonstrate that common
             task-fMRI measures are not currently suitable for brain
             biomarker discovery or individual differences research. We
             review how this state of affairs came to be and highlight
             avenues for improving task-fMRI reliability.},
   Doi = {10.1101/681700},
   Key = {fds350920}
}

@article{fds350921,
   Author = {Kim, MJ and Elliott, ML and d'Arbeloff, TC and Knodt, AR and Radtke, SR and Brigidi, BD and Hariri, AR},
   Title = {Microstructural integrity of white matter moderates an
             association between childhood adversity and adult trait
             anger.},
   Journal = {Aggressive Behavior},
   Volume = {45},
   Number = {3},
   Pages = {310-318},
   Year = {2019},
   Month = {May},
   url = {http://dx.doi.org/10.1002/ab.21820},
   Abstract = {Amongst a number of negative life sequelae associated with
             childhood adversity is the later expression of a higher
             dispositional tendency to experience anger and frustration
             to a wide range of situations (i.e., trait anger). We
             recently reported that an association between childhood
             adversity and trait anger is moderated by individual
             differences in both threat-related amygdala activity and
             executive control-related dorsolateral prefrontal cortex
             (dlPFC) activity, wherein individuals with relatively low
             amygdala and high dlPFC activity do not express higher trait
             anger even when having experienced childhood adversity.
             Here, we examine possible structural correlates of this
             functional dynamic using diffusion magnetic resonance
             imaging data from 647 young adult men and women volunteers.
             Specifically, we tested whether the degree of white matter
             microstructural integrity as indexed by fractional
             anisotropy modulated the association between childhood
             adversity and trait anger. Our analyses revealed that higher
             microstructural integrity of multiple pathways was
             associated with an attenuated link between childhood
             adversity and adult trait anger. Amongst these pathways was
             the uncinate fasciculus (UF; ΔR 2  = 0.01), which not
             only provides a major anatomical link between the amygdala
             and prefrontal cortex but also is associated with individual
             differences in regulating negative emotion through top-down
             cognitive reappraisal. These findings suggest that higher
             microstructural integrity of distributed white matter
             pathways including but not limited to the UF may represent
             an anatomical foundation serving to buffer against the
             expression of childhood adversity as later trait anger,
             which is itself associated with multiple negative health
             outcomes.},
   Doi = {10.1002/ab.21820},
   Key = {fds350921}
}

@article{fds341341,
   Author = {Elliott, ML and Knodt, AR and Cooke, M and Kim, MJ and Melzer, TR and Keenan, R and Ireland, D and Ramrakha, S and Poulton, R and Caspi, A and Moffitt, TE and Hariri, AR},
   Title = {General functional connectivity: Shared features of
             resting-state and task fMRI drive reliable and heritable
             individual differences in functional brain
             networks.},
   Journal = {Neuroimage},
   Volume = {189},
   Pages = {516-532},
   Year = {2019},
   Month = {April},
   url = {http://dx.doi.org/10.1016/j.neuroimage.2019.01.068},
   Abstract = {Intrinsic connectivity, measured using resting-state fMRI,
             has emerged as a fundamental tool in the study of the human
             brain. However, due to practical limitations, many studies
             do not collect enough resting-state data to generate
             reliable measures of intrinsic connectivity necessary for
             studying individual differences. Here we present general
             functional connectivity (GFC) as a method for leveraging
             shared features across resting-state and task fMRI and
             demonstrate in the Human Connectome Project and the Dunedin
             Study that GFC offers better test-retest reliability than
             intrinsic connectivity estimated from the same amount of
             resting-state data alone. Furthermore, at equivalent scan
             lengths, GFC displayed higher estimates of heritability than
             resting-state functional connectivity. We also found that
             predictions of cognitive ability from GFC generalized across
             datasets, performing as well or better than resting-state or
             task data alone. Collectively, our work suggests that GFC
             can improve the reliability of intrinsic connectivity
             estimates in existing datasets and, subsequently, the
             opportunity to identify meaningful correlates of individual
             differences in behavior. Given that task and resting-state
             data are often collected together, many researchers can
             immediately derive more reliable measures of intrinsic
             connectivity through the adoption of GFC rather than solely
             using resting-state data. Moreover, by better capturing
             heritable variation in intrinsic connectivity, GFC
             represents a novel endophenotype with broad applications in
             clinical neuroscience and biomarker discovery.},
   Doi = {10.1016/j.neuroimage.2019.01.068},
   Key = {fds341341}
}

@article{fds350922,
   Author = {d'Arbeloff, T and Elliott, ML and Knodt, AR and Melzer, TR and Keenan,
             R and Ireland, D and Ramrakha, S and Poulton, R and Anderson, T and Caspi,
             A and Moffitt, TE and Hariri, AR},
   Title = {White matter hyperintensities are common in midlife and
             already associated with cognitive decline.},
   Journal = {Brain Communications},
   Volume = {1},
   Number = {1},
   Pages = {fcz041},
   Year = {2019},
   Month = {January},
   url = {http://dx.doi.org/10.1093/braincomms/fcz041},
   Abstract = {White matter hyperintensities proliferate as the brain ages
             and are associated with increased risk for cognitive decline
             as well as Alzheimer's disease and related dementias. As
             such, white matter hyperintensities have been targeted as a
             surrogate biomarker in intervention trials with older
             adults. However, it is unclear at what stage of aging white
             matter hyperintensities begin to relate to cognition and if
             they may be a viable target for early prevention. In the
             Dunedin Study, a population-representative cohort followed
             since birth, we measured white matter hyperintensities in
             843 45-year-old participants using T2-weighted magnetic
             resonance imaging and we assessed cognitive decline from
             childhood to midlife. We found that white matter
             hyperintensities were common at age 45 and that white matter
             hyperintensity volume was modestly associated with both
             lower childhood (ß = -0.08, P = 0.013) and adult IQ
             (ß=-0.15, P < 0.001). Moreover, white matter
             hyperintensity volume was associated with greater cognitive
             decline from childhood to midlife (ß=-0.09, P < 0.001).
             Our results demonstrate that a link between white matter
             hyperintensities and early signs of cognitive decline is
             detectable decades before clinical symptoms of dementia
             emerge. Thus, white matter hyperintensities may be a useful
             surrogate biomarker for identifying individuals in midlife
             at risk for future accelerated cognitive decline and
             selecting participants for dementia prevention
             trials.},
   Doi = {10.1093/braincomms/fcz041},
   Key = {fds350922}
}

@article{fds350923,
   Author = {Avinun, R and Nevo, A and Knodt, AR and Elliott, ML and Hariri,
             AR},
   Title = {Replication in Imaging Genetics: The Case of Threat-Related
             Amygdala Reactivity.},
   Journal = {Biological Psychiatry},
   Volume = {84},
   Number = {2},
   Pages = {148-159},
   Year = {2018},
   Month = {July},
   url = {http://dx.doi.org/10.1016/j.biopsych.2017.11.010},
   Abstract = {<h4>Background</h4>Low replication rates are a concern in
             most, if not all, scientific disciplines. In psychiatric
             genetics specifically, targeting intermediate brain
             phenotypes, which are more closely associated with putative
             genetic effects, was touted as a strategy leading to
             increased power and replicability. In the current study, we
             attempted to replicate previously published associations
             between single nucleotide polymorphisms and threat-related
             amygdala reactivity, which represents a robust brain
             phenotype not only implicated in the pathophysiology of
             multiple disorders, but also used as a biomarker of future
             risk.<h4>Methods</h4>We conducted a literature search for
             published associations between single nucleotide
             polymorphisms and threat-related amygdala reactivity and
             found 37 unique findings. Our replication sample consisted
             of 1117 young adult volunteers (629 women, mean age 19.72 ±
             1.25 years) for whom both genetic and functional magnetic
             resonance imaging data were available.<h4>Results</h4>Of the
             37 unique associations identified, only three replicated as
             previously reported. When exploratory analyses were
             conducted with different model parameters compared to the
             original findings, significant associations were identified
             for 28 additional studies: eight of these were for a
             different contrast/laterality; five for a different gender
             and/or race/ethnicity; and 15 in the opposite direction and
             for a different contrast, laterality, gender, and/or
             race/ethnicity. No significant associations, regardless of
             model parameters, were detected for six studies. Notably,
             none of the significant associations survived correction for
             multiple comparisons.<h4>Conclusions</h4>We discuss these
             patterns of poor replication with regard to the general
             strategy of targeting intermediate brain phenotypes in
             genetic association studies and the growing importance of
             advancing the replicability of imaging genetics
             findings.},
   Doi = {10.1016/j.biopsych.2017.11.010},
   Key = {fds350923}
}

@article{fds350924,
   Author = {Elliott, M and Knodt, A and Cooke, M and Kim, J and Melzer, T and Keenan,
             R and Ireland, D and Ramrakha, S and Poulton, R and Caspi, A and Moffitt,
             T and Hariri, A},
   Title = {General Functional Connectivity: shared features of
             resting-state and task fMRI drive reliable and heritable
             individual differences in functional brain
             networks},
   Year = {2018},
   Month = {May},
   url = {http://dx.doi.org/10.1101/330530},
   Abstract = {Intrinsic connectivity, measured using resting-state fMRI,
             has emerged as a fundamental tool in the study of the human
             brain. However, due to practical limitations, many studies
             do not collect enough resting-state data to generate
             reliable measures of intrinsic connectivity necessary for
             studying individual differences. Here we present general
             functional connectivity (GFC) as a method for leveraging
             shared features across resting-state and task fMRI and
             demonstrate in the Human Connectome Project and the Dunedin
             Study that GFC offers better test-retest reliability than
             intrinsic connectivity estimated from the same amount of
             resting-state data alone. Furthermore, at equivalent scan
             lengths, GFC displays higher heritability on average than
             resting-state functional connectivity. We also show that
             predictions of cognitive ability from GFC generalize across
             datasets, performing as well or better than resting-state or
             task data alone. Collectively, our work suggests that GFC
             can improve the reliability of intrinsic connectivity
             estimates in existing datasets and, subsequently, the
             opportunity to identify meaningful correlates of individual
             differences in behavior. Given that task and resting-state
             data are often collected together, many researchers can
             immediately derive more reliable measures of intrinsic
             connectivity through the adoption of GFC rather than solely
             using resting-state data. Moreover, by better capturing
             heritable variation in intrinsic connectivity, GFC
             represents a novel endophenotype with broad applications in
             clinical neuroscience and biomarker discovery.},
   Doi = {10.1101/330530},
   Key = {fds350924}
}

@article{fds340304,
   Author = {Elliott, ML and Romer, A and Knodt, AR and Hariri,
             AR},
   Title = {A Connectome Wide Functional Signature of Transdiagnostic
             Risk for Mental Illness},
   Journal = {Biological Psychiatry},
   Volume = {84},
   Number = {6},
   Pages = {452-459},
   Year = {2018},
   Month = {April},
   url = {http://dx.doi.org/10.1016/j.biopsych.2018.03.012},
   Abstract = {Background High rates of comorbidity, shared risk, and
             overlapping therapeutic mechanisms have led psychopathology
             research towards transdiagnostic dimensional investigations
             of clustered symptoms. One influential framework accounts
             for these transdiagnostic phenomena through a single general
             factor, sometimes referred to as the ‘p’ factor,
             associated with risk for all common forms of mental illness.
             Methods Here we build on past research identifying unique
             structural neural correlates of the p factor by conducting a
             data-driven analysis of connectome wide intrinsic functional
             connectivity (n = 605). Results We demonstrate that higher p
             factor scores and associated risk for common mental illness
             maps onto hyper-connectivity between visual association
             cortex and both frontoparietal and default mode networks.
             Conclusions These results provide initial evidence that the
             transdiagnostic risk for common forms of mental illness is
             associated with patterns of inefficient connectome wide
             intrinsic connectivity between visual association cortex and
             networks supporting executive control and self-referential
             processes, networks which are often impaired across
             categorical disorders.},
   Doi = {10.1016/j.biopsych.2018.03.012},
   Key = {fds340304}
}

@article{fds350925,
   Author = {Elliott, M and Belsky, D and Anderson, K and Corcoran, D and Ge, T and Knodt, A and Prinz, J and Sugden, K and Williams, B and Ireland, D and Poulton, R and Caspi, A and Holmes, A and Moffitt, T and Hariri,
             A},
   Title = {A Polygenic Score for Higher Educational Attainment is
             Associated with Larger Brains},
   Year = {2018},
   Month = {March},
   url = {http://dx.doi.org/10.1101/287490},
   Abstract = {People who score higher on intelligence tests tend to have
             larger brains. Twin studies suggest the same genetic factors
             influence both brain size and intelligence. This has led to
             the hypothesis that genetics influence intelligence partly
             by contributing to development of larger brains. We tested
             this hypothesis with molecular genetic data using
             discoveries from a genome-wide association study (GWAS) of
             educational attainment, a correlate of intelligence. We
             analyzed genetic, brain imaging, and cognitive test data
             from the UK Biobank, the Dunedin Study, the Brain Genomics
             Superstruct Project (GSP), and the Duke Neurogenetics Study
             (DNS) (combined N=8,271). We measured genetics using
             polygenic scores based on published GWAS. We conducted
             meta-analysis to test associations among participants’
             genetics, total brain volume (i.e., brain size), and
             cognitive test performance. Consistent with previous
             findings, participants with higher polygenic scores achieved
             higher scores on cognitive tests, as did participants with
             larger brains. Participants with higher polygenic scores
             also had larger brains. We found some evidence that brain
             size partly mediated associations between participants’
             education polygenic scores and their cognitive test
             performance. Effect-sizes were larger in the
             population-based UK Biobank and Dunedin samples than in the
             GSP and DNS samples. Sensitivity analysis suggested this
             effect-size difference partly reflected restricted range of
             cognitive performance in the GSP and DNS samples.
             Recruitment and retention of population-representative
             samples should be a priority for neuroscience research.
             Findings suggest promise for studies integrating GWAS
             discoveries with brain imaging data to understand
             neurobiology linking genetics with individual differences in
             cognitive performance.},
   Doi = {10.1101/287490},
   Key = {fds350925}
}

@article{fds350926,
   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.<b>SIGNIFICANCE
             STATEMENT</b> 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 = {fds350926}
}

@article{fds350927,
   Author = {Elliott, M and Romer, A and Knodt, A and Hariri, A},
   Title = {A Connectome Wide Functional Signature of Transdiagnostic
             Risk for Mental Illness},
   Year = {2017},
   Month = {September},
   url = {http://dx.doi.org/10.1101/196220},
   Abstract = {<h4>Background</h4> High rates of comorbidity, shared risk,
             and overlapping therapeutic mechanisms have led
             psychopathology research towards transdiagnostic dimensional
             investigations of clustered symptoms. One influential
             framework accounts for these transdiagnostic phenomena
             through a single general factor, sometimes referred to as
             the ‘p’ factor, associated with risk for all common
             forms of mental illness. <h4>Methods</h4> Here we build on
             past research identifying unique structural neural
             correlates of the p factor by conducting a data-driven
             analysis of connectome wide intrinsic functional
             connectivity (n = 605). <h4>Results</h4> We demonstrate that
             higher p factor scores and associated risk for common mental
             illness maps onto hyper-connectivity between visual
             association cortex and both frontoparietal and default mode
             networks. <h4>Conclusions</h4> These results provide initial
             evidence that the transdiagnostic risk for common forms of
             mental illness is associated with patterns of inefficient
             connectome wide intrinsic connectivity between visual
             association cortex and networks supporting executive control
             and self-referential processes, networks which are often
             impaired across categorical disorders.},
   Doi = {10.1101/196220},
   Key = {fds350927}
}

@article{fds358355,
   Author = {Gregory, M and Eisenberg, D and Elliott, M and Czarapata, J and Hegarty,
             C and Ianni, A and Kohn, P and Apud, J and Berman, K},
   Title = {Connectome-Wide Association of Resting fMRI With Dopamine
             Functioning in Patients With Schizophrenia and Healthy
             Adults},
   Journal = {Neuropsychopharmacology},
   Volume = {41},
   Pages = {S224-S225},
   Year = {2016},
   Month = {December},
   Key = {fds358355}
}

@article{fds358356,
   Author = {Elliott, M},
   Title = {A Data-Driven Exploration of the Functional Connectome in
             Williams Syndrome},
   Journal = {Biological Psychiatry},
   Volume = {79},
   Number = {9},
   Pages = {216S-217S},
   Year = {2016},
   Month = {May},
   Key = {fds358356}
}

@article{fds350928,
   Author = {Beim, JA and Elliott, M and Oxenham, AJ and Wojtczak,
             M},
   Title = {Stimulus Frequency Otoacoustic Emissions Provide No Evidence
             for the Role of Efferents in the Enhancement
             Effect.},
   Journal = {Journal of the Association for Research in Otolaryngology :
             Jaro},
   Volume = {16},
   Number = {5},
   Pages = {613-629},
   Year = {2015},
   Month = {October},
   url = {http://dx.doi.org/10.1007/s10162-015-0534-8},
   Abstract = {Auditory enhancement refers to the perceptual phenomenon
             that a target sound is heard out more readily from a
             background sound if the background is presented alone first.
             Here we used stimulus-frequency otoacoustic emissions
             (SFOAEs) to test the hypothesis that activation of the
             medial olivocochlear efferent system contributes to auditory
             enhancement effects. The SFOAEs were used as a tool to
             measure changes in cochlear responses to a target component
             and the neighboring components of a multitone background
             between conditions producing enhancement and conditions
             producing no enhancement. In the "enhancement" condition,
             the target and multitone background were preceded by a
             precursor stimulus with a spectral notch around the signal
             frequency; in the control (no-enhancement) condition, the
             target and multitone background were presented without the
             precursor. In an experiment using a wideband multitone
             stimulus known to produce significant psychophysical
             enhancement effects, SFOAEs showed no changes consistent
             with enhancement, but some aspects of the results indicated
             possible contamination of the SFOAE magnitudes by the
             activation of the middle-ear-muscle reflex. The same SFOAE
             measurements performed using narrower-band stimuli at lower
             sound levels also showed no SFOAE changes consistent with
             either absolute or relative enhancement despite robust
             psychophysical enhancement effects observed in the same
             listeners with the same stimuli. The results suggest that
             cochlear efferent control does not play a significant role
             in auditory enhancement effects.},
   Doi = {10.1007/s10162-015-0534-8},
   Key = {fds350928}
}


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