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Image processing and analysis methods for the Adolescent Brain Cognitive Development Study.

ABSTRACT: The Adolescent Brain Cognitive Development (ABCD) Study is an ongoing, nationwide study of the effects of environmental influences on behavioral and brain development in adolescents. The main objective of the study is to recruit and assess over eleven thousand 9-10-year-olds and follow them over the course of 10 years to characterize normative brain and cognitive development, the many factors that influence brain development, and the effects of those factors on mental health and other outcomes. The study employs state-of-the-art multimodal brain imaging, cognitive and clinical assessments, bioassays, and careful assessment of substance use, environment, psychopathological symptoms, and social functioning. The data is a resource of unprecedented scale and depth for studying typical and atypical development. The aim of this manuscript is to describe the baseline neuroimaging processing and subject-level analysis methods used by ABCD. Processing and analyses include modality-specific corrections for distortions and motion, brain segmentation and cortical surface reconstruction derived from structural magnetic resonance imaging (sMRI), analysis of brain microstructure using diffusion MRI (dMRI), task-related analysis of functional MRI (fMRI), and functional connectivity analysis of resting-state fMRI. This manuscript serves as a methodological reference for users of publicly shared neuroimaging data from the ABCD Study.

SUBMITTER: Hagler DJ

PROVIDER: S-EPMC6981278 | biostudies-literature | 2019 Nov

REPOSITORIES: biostudies-literature

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Image processing and analysis methods for the Adolescent Brain Cognitive Development Study.

Hagler Donald J DJ Hatton SeanN S Cornejo M Daniela MD Makowski Carolina C Fair Damien A DA Dick Anthony Steven AS Sutherland Matthew T MT Casey B J BJ Barch Deanna M DM Harms Michael P MP Watts Richard R Bjork James M JM Garavan Hugh P HP Hilmer Laura L Pung Christopher J CJ Sicat Chelsea S CS Kuperman Joshua J Bartsch Hauke H Xue Feng F Heitzeg Mary M MM Laird Angela R AR Trinh Thanh T TT Gonzalez Raul R Tapert Susan F SF Riedel Michael C MC Squeglia Lindsay M LM Hyde Luke W LW Rosenberg Monica D MD Earl Eric A EA Howlett Katia D KD Baker Fiona C FC Soules Mary M Diaz Jazmin J de Leon Octavio Ruiz OR Thompson Wesley K WK Neale Michael C MC Herting Megan M Sowell Elizabeth R ER Alvarez Ruben P RP Hawes Samuel W SW Sanchez Mariana M Bodurka Jerzy J Breslin Florence J FJ Morris Amanda Sheffield AS Paulus Martin P MP Simmons W Kyle WK Polimeni Jonathan R JR van der Kouwe Andre A Nencka Andrew S AS Gray Kevin M KM Pierpaoli Carlo C Matochik John A JA Noronha Antonio A Aklin Will M WM Conway Kevin K Glantz Meyer M Hoffman Elizabeth E Little Roger R Lopez Marsha M Pariyadath Vani V Weiss Susan Rb SR Wolff-Hughes Dana L DL DelCarmen-Wiggins Rebecca R Feldstein Ewing Sarah W SW Miranda-Dominguez Oscar O Nagel Bonnie J BJ Perrone Anders J AJ Sturgeon Darrick T DT Goldstone Aimee A Pfefferbaum Adolf A Pohl Kilian M KM Prouty Devin D Uban Kristina K Bookheimer Susan Y SY Dapretto Mirella M Galvan Adriana A Bagot Kara K Giedd Jay J Infante M Alejandra MA Jacobus Joanna J Patrick Kevin K Shilling Paul D PD Desikan Rahul R Li Yi Y Sugrue Leo L Banich Marie T MT Friedman Naomi N Hewitt John K JK Hopfer Christian C Sakai Joseph J Tanabe Jody J Cottler Linda B LB Nixon Sara Jo SJ Chang Linda L Cloak Christine C Ernst Thomas T Reeves Gloria G Kennedy David N DN Heeringa Steve S Peltier Scott S Schulenberg John J Sripada Chandra C Zucker Robert A RA Iacono William G WG Luciana Monica M Calabro Finnegan J FJ Clark Duncan B DB Lewis David A DA Luna Beatriz B Schirda Claudiu C Brima Tufikameni T Foxe John J JJ Freedman Edward G EG Mruzek Daniel W DW Mason Michael J MJ Huber Rebekah R McGlade Erin E Prescot Andrew A Renshaw Perry F PF Yurgelun-Todd Deborah A DA Allgaier Nicholas A NA Dumas Julie A JA Ivanova Masha M Potter Alexandra A Florsheim Paul P Larson Christine C Lisdahl Krista K Charness Michael E ME Fuemmeler Bernard B Hettema John M JM Maes Hermine H HH Steinberg Joel J Anokhin Andrey P AP Glaser Paul P Heath Andrew C AC Madden Pamela A PA Baskin-Sommers Arielle A Constable R Todd RT Grant Steven J SJ Dowling Gayathri J GJ Brown Sandra A SA Jernigan Terry L TL Dale Anders M AM

NeuroImage 20190812

The Adolescent Brain Cognitive Development (ABCD) Study is an ongoing, nationwide study of the effects of environmental influences on behavioral and brain development in adolescents. The main objective of the study is to recruit and assess over eleven thousand 9-10-year-olds and follow them over the course of 10 years to characterize normative brain and cognitive development, the many factors that influence brain development, and the effects of those factors on mental health and other outcomes. ...[more]

PMID: 31415884

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Project description:BackgroundAdolescence is a critical developmental stage. A key challenge is to characterize how variation in adolescent brain organization relates to psychosocial and environmental influences.MethodsWe used canonical correlation analysis to discover distinct patterns of covariation between measures of brain organization (brain morphometry, intracortical myelination, white matter integrity, and resting-state functional connectivity) and individual, psychosocial, and environmental factors in a nationally representative U.S. sample of 9623 individuals (aged 9-10 years, 49% female) participating in the Adolescent Brain and Cognitive Development (ABCD) study.ResultsThese analyses identified 14 reliable modes of brain-behavior-environment covariation (canonical rdiscovery = .21 to .49, canonical rtest = .10 to .39, pfalse discovery rate corrected < .0001). Across modes, neighborhood environment, parental characteristics, quality of family life, perinatal history, cardiometabolic health, cognition, and psychopathology had the most consistent and replicable associations with multiple measures of brain organization; positive and negative exposures converged to form patterns of psychosocial advantage or adversity. These showed modality-general, respectively positive or negative, associations with brain structure and function with little evidence of regional specificity. Nested within these cross-modal patterns were more specific associations between prefrontal measures of morphometry, intracortical myelination, and functional connectivity with affective psychopathology, cognition, and family environment.ConclusionsWe identified clusters of exposures that showed consistent modality-general associations with global measures of brain organization. These findings underscore the importance of understanding the complex and intertwined influences on brain organization and mental function during development and have the potential to inform public health policies aiming toward interventions to improve mental well-being.

Project description:BackgroundChildhood obsessive-compulsive symptoms (OCSs) are common and can be an early risk marker for obsessive-compulsive disorder. The Adolescent Brain and Cognitive Development (ABCD) Study provides a unique opportunity to characterize OCSs in a large normative sample of school-age children and to explore corticostriatal and task-control circuits implicated in pediatric obsessive-compulsive disorder.MethodsThe ABCD Study acquired data from 9- and 10-year-olds (N = 11,876). Linear mixed-effects models probed associations between OCSs (Child Behavior Checklist) and cognition (NIH Toolbox), brain structure (subcortical volume, cortical thickness), white matter (diffusion tensor imaging), and resting-state functional connectivity.ResultsOCS scores showed good psychometric properties and high prevalence, and they were related to familial/parental factors, including family conflict. Higher OCS scores related to better cognitive performance (β = .06, t9966.60 = 6.28, p < .001, ηp2= .01), particularly verbal, when controlling for attention-deficit/hyperactivity disorder, which related to worse performance. OCSs did not significantly relate to brain structure but did relate to lower superior corticostriatal tract fractional anisotropy (β = -.03, t = -3.07, p = .002, ηp2= .02). Higher OCS scores were related to altered functional connectivity, including weaker connectivity within the dorsal attention network (β = -.04, t7262.87 = -3.71, p < .001, ηp2= .002) and weaker dorsal attention-default mode anticorrelation (β = .04, t7251.95 = 3.94, p < .001, ηp2 = .002). Dorsal attention-default mode connectivity predicted OCS scores at 1 year (β = -.04, t2407.61 = -2.23, p = .03, ηp2 = .03).ConclusionsOCSs are common and may persist throughout childhood. Corticostriatal connectivity and attention network connectivity are likely mechanisms in the subclinical-to-clinical spectrum of OCSs. Understanding correlates and mechanisms of OCSs may elucidate their role in childhood psychiatric risk and suggest potential utility of neuroimaging, e.g., dorsal attention-default mode connectivity, for identifying children at increased risk for obsessive-compulsive disorder.

Project description:BackgroundChildhood psychotic-like experiences (PLEs) often precede the development of later severe psychopathology. This study examined whether childhood PLEs are associated with several psychopathology-related polygenic scores (PGSs) and additionally examined possible neural and behavioral mechanisms.MethodsAdolescent Brain Cognitive Development Study baseline data from children with European ancestry (n = 4650, ages 9-10 years, 46.8% female) were used to estimate associations between PLEs (i.e., both total and presence of significantly distressing) and PGSs for psychopathology (i.e., schizophrenia, psychiatric cross-disorder risk, PLEs) and related phenotypes (i.e., educational attainment [EDU], birth weight, inflammation). We also assessed whether variability in brain structure indices (i.e., volume, cortical thickness, surface area) and behaviors proximal to PGSs (e.g., cognition for EDU) indirectly linked PGSs to PLEs using mediational models.ResultsTotal and significantly distressing PLEs were associated with EDU and cross-disorder PGSs (all %ΔR2s = 0.202%-0.660%; false discovery rate-corrected ps < .006). Significantly distressing PLEs were also associated with higher schizophrenia and PLE PGSs (both %ΔR2 = 0.120%-0.216%; false discovery rate-corrected ps < .03). There was evidence that global brain volume metrics and cognitive performance indirectly linked EDU PGS to PLEs (estimated proportion mediated = 3.33%-32.22%).ConclusionsTotal and significantly distressing PLEs were associated with genomic risk indices of broad-spectrum psychopathology risk (i.e., EDU and cross-disorder PGSs). Significantly distressing PLEs were also associated with genomic risk for psychosis (i.e., schizophrenia, PLEs). Global brain volume metrics and PGS-proximal behaviors represent promising putative intermediary phenotypes that may indirectly link genomic risk to psychopathology. Broadly, polygenic scores derived from genome-wide association studies of adult samples generalize to indices of psychopathology risk among children.

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Image processing and analysis methods for the Adolescent Brain Cognitive Development Study.

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Image processing and analysis methods for the Adolescent Brain Cognitive Development Study.

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