Scientific Publications

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Internalising disorders are highly prevalent emotional dysregulations during preadolescence but clinical decision-making is hampered by high heterogeneity. During this period impulsivity represents a major risk factor for psychopathological trajectories and may act on this heterogeneity given the controversial anxiety-impulsivity relationships. However, how impulsivity contributes to the heterogeneous symptomatology, neurobiology, neurocognition and clinical trajectories in preadolescent internalising disorders remains unclear.

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Screen use is a known risk factor for adverse physical and mental health outcomes during childhood and adolescence. Moreover, racial/ethnic disparity in screen use persists among adolescents. However, limited studies have characterized the population sharing similar longitudinal patterns of screen use from childhood to adolescence. This study will identify and characterize the subgroups of adolescents sharing similar trajectories of screen use from childhood to adolescence. Study participants of the Adolescent Brain Cognitive Development Study (2016-2021) in the U.S with non-missing responses on self-reported screen use at each year of the study were included in the analysis. Growth mixture modeling was used to identify the optimal number of subgroups of adolescents with similar trajectories. Subsequently, socio-demographic characteristics, familial background, and perceived racism and discrimination during childhood was assessed for each subgroup population. Perceived discrimination was measured using the Perceived Discrimination Scale. There were two major subgroups of individuals sharing similar trajectories of screen use: Drastically Increasing group (N = 1333); Gradually Increasing group (N = 10336). Higher proportions of the Drastically Increasing group were racial/ethnic minorities (70%) as compared to the Gradually Increasing group (45%). Moreover, the Drastically Increasing group had higher proportions of individuals reporting perceived racism and discrimination during childhood.

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The study aim was to determine whether (A) differences in executive function (EF) and cognition precede weight gain or (B) weight gain causes changes to EF and cognition.

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Puberty is a key event in adolescent development that involves significant, hormone-driven changes to many aspects of physiology including the brain. Understanding how the brain responds during this time period is important for evaluating neuronal developments that affect mental health throughout adolescence and the adult lifespan. This study examines diffusion MRI scans from the cross-sectional ABCD Study baseline cohort, a large multi-site study containing thousands of participants, to describe the relationship between pubertal development and brain microstructure. Using advanced, 3-tissue constrained spherical deconvolution methods, this study is able to describe multiple tissue compartments beyond only white matter (WM) axonal qualities. After controlling for age, sex, brain volume, subject handedness, scanning site, and sibling relationships, we observe a positive relationship between an isotropic, intracellular diffusion signal fraction and pubertal development across a majority of regions of interest (ROIs) in the WM skeleton. We also observe regional effects from an intracellular anisotropic signal fraction compartment and extracellular isotropic free water-like compartment in several ROIs. This cross-sectional work suggests that changes in pubertal status are associated with a complex response from brain tissue that cannot be completely described by traditional methods focusing only on WM axonal properties.

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Family cultural values that emphasize support, loyalty, and obligation to the family are associated with lower psychopathology in Hispanic/Latino/a youth, but there is a need to understand the implications of family cultural values for youth development in racially/ethnically heterogeneous samples. This study examined phenotypic associations between parent- and youth-reported family cultural values in late childhood on youth internalizing and externalizing symptoms in early adolescence, and whether family cultural values moderated genetic and environmental influences on psychopathology symptoms. The sample comprised 10,335 children (M=12.89 years; 47.9% female; 20.3% Hispanic/Latino/a, 15.0% Black, 2.1% Asian, 10.5% other) and their parents from the Adolescent Brain Cognitive Development (ABCD) Study, and biometric models were conducted in the twin subsample (n = 1,042 twin pairs; 43.3% monozygotic). Parents and youth reported on their family cultural values using the Mexican American Cultural Values Scale at youth age 11-12, and parents reported on youth internalizing and externalizing symptoms using the Child Behavior Checklist at youth ages 11-12 and 12-13. Greater parent- and youth-reported family cultural values predicted fewer youth internalizing and externalizing symptoms. Biometric models indicated that higher parent-reported family cultural values increased the nonshared environmental influences on externalizing symptoms whereas youth-reported family cultural values decreased the nonshared environmental influences on internalizing symptoms. This study highlights the need for behavior genetic research to consider a diverse range of cultural contexts to better understand the etiology of youth psychopathology.

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Adolescents, particularly racial and ethnic minorities, are at increased risk for neighborhood threat and violence exposure, which impacts behavioral and neural outcomes. Caregiver support is associated with healthy socioemotional adjustment and self-regulatory and coping behaviors; however, it remains unclear whether caregiver support, specifically, consolation, can moderate the behavioral and neural impacts of neighborhood threat.

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Pediatric overweight/obesity can lead to sleep-disordered breathing (SDB), abnormal neurological and cognitive development, and psychiatric problems, but the associations and interactions between these factors have not been fully explored. Therefore, we investigated the associations between body mass index (BMI), SDB, psychiatric and cognitive measures, and brain morphometry in 8484 children 9-11 years old using the Adolescent Brain Cognitive Development dataset. BMI was positively associated with SDB, and both were negatively correlated with cortical thickness in lingual gyrus and lateral orbitofrontal cortex, and cortical volumes in postcentral gyrus, precentral gyrus, precuneus, superior parietal lobule, and insula. Mediation analysis showed that SDB partially mediated the effect of overweight/obesity on these brain regions. Dimensional psychopathology (including aggressive behavior and externalizing problem) and cognitive function were correlated with BMI and SDB. SDB and cortical volumes in precentral gyrus and insula mediated the correlations between BMI and externalizing problem and matrix reasoning ability. Comparisons by sex showed that obesity and SDB had a greater impact on brain measures, cognitive function, and mental health in girls than in boys. These findings suggest that preventing childhood obesity will help decrease SDB symptom burden, abnormal neurological and cognitive development, and psychiatric problems.

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A growing body of neuroimaging studies has reported common neural abnormalities among mental disorders in adults. However, it is unclear whether the distinct disorder-specific mechanisms operate during adolescence despite the overlap among disorders.

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The objective of this study was to determine the association between cyberbullying and eating disorder symptoms in a national sample of 10-14-year-old early adolescents.

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Earlier pubertal timing is an important predictor of emotional and behavioral problems during adolescence. The current study undertook a comprehensive investigation of whether the social environment can buffer or amplify the associations between pubertal timing and emotional and behavioral problems.

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Early pubertal timing is associated with youth mental health problems, with association amplified or mitigated by characteristics of the residential neighborhood. Yet, limited research simultaneously examines the roles of neighborhood context and biological sex in this association. This study fills this research gap by examining sex-specific associations between pubertal timing and neighborhood income with youth mental health problems (internalizing and externalizing symptoms) in a longitudinal cohort of early adolescents in the United States (US). Participants were 9201 youth aged 9 or 10 years from the Adolescent Brain Cognitive Development Study. Pubertal timing was the average of parent- and youth-reported pubertal status standardized within sex and age. Outcome variables were youths’ internalizing and externalizing symptoms assessed at 1-year follow-up via parent survey. We evaluated interaction effects between pubertal timing and neighborhood income in a series of sex-stratified linear mixed effect models, adjusted for family and personal sociodemographic characteristics. In girls, earlier pubertal timing was associated with more internalizing (β = 0.06, p < 0.001) and externalizing problems (β = 0.07, p < 0.001) at 1-year follow-up, not moderated by neighborhood income. In boys, earlier pubertal timing was associated with more externalizing problems among youth living in high-income neighborhoods, but not among those in low-income neighborhoods (interaction-p = 0.006). Results suggest that pubertal timing may affect youth mental health differentially in boys and girls, depending on the neighborhood contexts. These findings highlight the importance of both biological and social forces in shaping adolescent mental health and, thus, have public health and clinical implications for health promotion.

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Aspects of the built environment relate to health factors and equity in living conditions, and may contribute to racial, ethnic, or economic health disparities. For example, urbanicity is linked with negative factors including exposure to gray space (e.g., impervious surfaces such as concrete, streets, or rooftops). While there is existing research on access to green space and urbanicity on some mental health and cognitive outcomes, there is limited research on the presence of space linked with cognitive functioning in youth. The goal of this study was to investigate the link between gray space and amygdala-default mode network (DMN) connectivity.

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The goal of this study is to investigate the cross-sectional and longitudinal relationships between clustered lifestyle risk factors (sleep, physical activity, body mass index [BMI], and screen time) and neurodevelopment over the early adolescent period.

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Deep learning on resting-state functional MRI (rs-fMRI) has shown great success in predicting a single cognition or mental disease. Nevertheless, cognitive functions or mental diseases may share neural mechanisms that can benefit their prediction/classification. We propose a multi-level and joint attention (ML-Joint-Att) network to learn high-order representations of brain functional connectivities that are specific and shared across multiple tasks. We design the ML-Joint-Att network with edge and node convolutional operators, an adaptive inception module, and three attention modules, including network-wise, region-wise, and region-wise joint attention modules. The adaptive inception learns brain functional connectivity at multiple spatial scales. The network-wise and region-wise attention modules take the multi-scale functional connectivities as input and learn features at the network and regional levels for individual tasks. Moreover, the joint attention module is designed as region-wise joint attention to learn shared brain features that contribute to and compensate for the prediction of multiple tasks. We employed the Adolescent Brain Cognitive Development (ABCD) dataset (n =9092) to evaluate the ML-Joint-Att network for the prediction of cognitive flexibility and inhibition. Our experiments demonstrated the usefulness of the three attention modules and identified brain functional connectivities and regions specific and common between cognitive flexibility and inhibition. In particular, the joint attention module can significantly improve the prediction of both cognitive functions. Moreover, leave-one-site cross-validation showed that the ML-Joint-Att network is robust to independent samples obtained from different sites of the ABCD study. Our network outperformed existing machine learning techniques, including Brain Bias Set (BBS), spatio-temporal graph convolution network (ST-GCN), and BrainNetCNN. We demonstrated the generalization of our method to other applications, such as the prediction of fluid intelligence and crystallized intelligence, which also outperformed the ST-GCN and BrainNetCNN.

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Our understanding of the genetics of the human cerebral cortex is limited both in terms of the diversity and the anatomical granularity of brain structural phenotypes. Here we conducted a genome-wide association meta-analysis of 13 structural and diffusion magnetic resonance imaging-derived cortical phenotypes, measured globally and at 180 bilaterally averaged regions in 36,663 individuals and identified 4,349 experiment-wide significant loci. These phenotypes include cortical thickness, surface area, gray matter volume, measures of folding, neurite density and water diffusion. We identified four genetic latent structures and causal relationships between surface area and some measures of cortical folding. These latent structures partly relate to different underlying gene expression trajectories during development and are enriched for different cell types. We also identified differential enrichment for neurodevelopmental and constrained genes and demonstrate that common genetic variants associated with cortical expansion are associated with cephalic disorders. Finally, we identified complex interphenotype and inter-regional genetic relationships among the 13 phenotypes, reflecting the developmental differences among them. Together, these analyses identify distinct genetic organizational principles of the cortex and their correlates with neurodevelopment.

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Racial and ethnic discrimination are known stressors and are associated with negative psychological and physical health outcomes. Previous studies have found relationships between racial/ethnic discrimination and binge-eating disorder (BED), though they have mainly focused on adult populations. The aim of this study was to determine associations between racial/ethnic discrimination and BED in a large, national cohort study of early adolescents. We further sought to explore associations between the racial/ethnic discrimination perpetrator (students, teachers, or other adults) and BED.

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Crystallized abilities are skills used to solve problems based on experience, while fluid abilities are linked to reasoning without evoke prior knowledge. To what extent crystallized and fluid abilities involve dissociated or overlapping neural systems is debatable. Due to often deployed small sample sizes or different study settings in prior work, the neural basis of crystallized and fluid abilities in childhood remains largely unknown. Here we analyzed within and between network connectivity patterns from resting-state functional MRI of 2707 children between 9 and 10 years from the ABCD study. We hypothesized that differences in functional connectivity at the default mode network (DMN), ventral, and dorsal attentional networks (VAN, DAN) explain differences in fluid and crystallized abilities. We found that stronger between-network connectivity of the DMN and VAN, DMN and DAN, and VAN and DAN predicted crystallized abilities. Within-network connectivity of the DAN predicted both crystallized and fluid abilities. Our findings reveal that crystallized abilities rely on the functional coupling between attentional networks and the DMN, whereas fluid abilities are associated with a focal connectivity configuration at the DAN. Our study provides new evidence into the neural basis of child intelligence and calls for future comparative research in adulthood during neuropsychiatric diseases.

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Higher family income (FI) is associated with larger cortical gray matter volume and improved cognitive performance in children. However, little is known about the effects of FI on brain functional and structural connectivity. This cross-sectional study investigates the effects of FI on brain connectivity and cognitive performance in 9- to 11-years old children (n = 8739) from the Adolescent Brain Cognitive Development (ABCD) study. Lower FI was associated with decreased global functional connectivity density (gFCD) in the default-mode network (DMN), inferior and superior parietal cortices and in posterior cerebellum, and increased gFCD in motor, auditory, and extrastriate visual areas, and in subcortical regions both for girls and boys. Findings demonstrated high reproducibility in Discovery and Reproducibility samples. Cognitive performance partially mediated the association between FI and DMN connectivity, whereas DMN connectivity did not mediate the association between FI and cognitive performance. In contrast, there was no significant association between FI and structural connectivity. Findings suggest that poor cognitive performance, which likely reflects multiple factors (genetic, nutritional, the level and quality of parental interactions, and educational exposure [1]), contributes to reduced DMN functional connectivity in children from low-income families. Follow-up studies are needed to help clarify if this leads to reductions in structural connectivity as these children age.

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Our objective was to determine whether there is an association between adverse childhood experiences (ACEs) and lifetime history of early childhood mild head or neck injury and concussion in a nationally representative US cohort.

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Binge eating is a relatively common disordered eating behavior among children, and is associated with poor health outcomes. Executive function (EF)-higher order cognitive abilities related to planning and impulse control-may be implicated in both binge eating and pediatric obesity. Although EF deficits are evident among individuals with obesity and/or binge eating, findings are mixed across the lifespan.

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Sexual minorities, including children, are at increased risk for adverse mental health outcomes compared to their heterosexual peers, but longitudinal studies are needed to determine the factors that explain the associations between sexual minority identification and adverse mental health outcomes during this developmental period. We examined longitudinal associations between sexual orientation and mental health over 2 years in a US cohort of children (aged 9-10 at baseline) and two explanatory factors (increased social problems such as getting teased and decreased perceived school safety). We hypothesized that beginning to identify as gay/bisexual and consistently identifying as gay/bisexual would be associated with increases in internalizing (e.g. depression, anxiety) and externalizing (e.g. aggression) problems compared to consistently identifying as heterosexual, and these associations would be partially explained by increased social problems and decreased perceived school safety.

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Evidence shows that cyberbullying is an important risk factor for various adverse mental health outcomes, such as substance use. However, there is limited evidence from longitudinal studies that assessed whether cyberbullying victimization is associated with substance use initiation, especially among adolescent population.

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In a new study, Yun-Jun Sun, Barbara Sahakian et al. examined the relationship between childhood RfP and brain structure, cognition and mental wellbeing in adolescence. Using a sample of more than 10,000 young adolescents from the Adolescent Brain Cognitive Development (ABCD) cohort, the researchers assessed brain scans, cognitive test scores, academic performance, anxiety, stress, depression scores, and psychopathological behavior, including aggression and rule-breaking. They divided the adolescents into two groups: one with a RfP duration of 3–10 years and the other with 0–2.5 years. “Adolescence is the transition between being a child to becoming an adult and so interventions in childhood that are beneficial for cognition, school academic attainment and mental health are extremely important. Many mental health disorders begin in childhood or adolescence, so improving mental health during these developmental periods is crucial,” explains Sahakian, a joint first author of the paper.

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Binge eating disorder (BED) is the most common eating disorder, yet its genetic architecture remains largely unknown. Studying BED is challenging because it is often comorbid with obesity, a common and highly polygenic trait, and it is underdiagnosed in biobank data sets. To address this limitation, we apply a supervised machine-learning approach (using 822 cases of individuals diagnosed with BED) to estimate the probability of each individual having BED based on electronic medical records from the Million Veteran Program. We perform a genome-wide association study of individuals of African (n = 77,574) and European (n = 285,138) ancestry while controlling for body mass index to identify three independent loci near the HFE, MCHR2 and LRP11 genes and suggest APOE as a risk gene for BED. We identify shared heritability between BED and several neuropsychiatric traits, and implicate iron metabolism in the pathophysiology of BED. Overall, our findings provide insights into the genetics underlying BED and suggest directions for future translational research.

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Psychopathology in youth is highly prevalent and associated with psychopathology in adulthood. However, the developmental trajectories of psychopathology symptoms, including potential gender differences, are markedly underspecified. The present study employed a directed network approach to investigate longitudinal relationships and gender differences among eight transdiagnostic symptom domains across three years, in a homogenous age sample of youth participants (n = 6,414; mean baseline age = 10.0 years; 78.6% White; Adolescent Brain Cognitive Development study). Anxious/depressed problems and aggressive behaviors were central symptoms and most predictive of increases in other symptom clusters at later timepoints. Rule-breaking behaviors, aggressive behaviors, and withdrawn/depressed problems emerged as bridge symptoms between externalizing and internalizing problems. Results supported cascade models in which externalizing problems predicted future internalizing problems, but internalizing problems also significantly predicted future externalizing problems, which is contrary to cascade models. Network structure, symptom centrality, and patterns of bridge symptoms differed between female and male participants, suggesting gender differences in the developmental trajectories of youth psychopathology. Results provide new insights into symptom trajectories and associated gender differences that may provide promising pathways for understanding disorder (dis)continuity and co-occurrence. The central and bridge symptoms identified here may have important implications for screening and early intervention for youth psychopathology.

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Comorbidity is the rule rather than the exception for childhood and adolescent onset mental disorders, but we cannot predict its occurrence and do not know the neural mechanisms underlying comorbidity. We investigate if the effects of comorbid internalizing and externalizing disorders on anatomical differences represent a simple aggregate of the effects on each disorder and if these comorbidity-associated cortical surface differences relate to a distinct genetic underpinning.

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Adolescence is often associated with an increase in psychopathology. Although previous studies have examined how family environments and neural reward sensitivity separately play a role in youth’s emotional development, it remains unknown how they interact with each other in predicting youth’s internalizing symptoms. Therefore, the current research took a biopsychosocial approach to examine this question using two-wave longitudinal data of 9353 preadolescents (mean age = 9.93 years at T1; 51% boys) from the Adolescent Brain Cognitive Development study. Using mixed-effects models, results showed that higher family conflict predicted youth’s increased internalizing symptoms 1 year later, whereas greater ventral striatum (VS) activity during reward receipt predicted reduced internalizing symptoms over time. Importantly, there was an interaction effect between family conflict and VS activity. For youth who showed greater VS activation during reward receipt, high family conflict was more likely to predict increased internalizing symptoms. In contrast, youth with low VS activation during reward receipt showed high levels of internalizing symptoms regardless of family conflict. The findings suggest that youth’s neural reward sensitivity is a marker of susceptibility to adverse family environments and highlight the importance of cultivating supportive family environments where youth experience less general conflict within the family.

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Functional interactions and anatomic connections between brain regions form the connectome. Its mathematical representation in terms of a graph reflects the inherent neuroanatomical organization into structures and regions (nodes) that are interconnected through neural fiber tracts and/or interact functionally (edges). Without knowledge of the ground truth topology of the connectome, functional (directional or nondirectional) graphs represent estimates of signal correlations, from which underlying mechanisms and processes, such as development and aging, or neuropathologies, are difficult to unravel. Biologically meaningful simulations using synthetic graphs with controllable parameters can complement real data analyses and provide critical insights into mechanisms underlying the organization of the connectome. Generative models can be highly valuable tools for creating large datasets of synthetic graphs with known topological characteristics. However, for these graphs to be meaningful, the variation of model parameters needs to be driven by real data. This paper presents a novel, data-driven approach for tuning the parameters of the generative Lancichinetti-Fortunato-Radicchi (LFR) model, using a large dataset of connectomes (n = 5566) estimated from resting-state fMRI from early adolescents in the historically large Adolescent Brain Cognitive Development Study (ABCD). It also presents an application, i.e., simulations using the LFR, to generate large datasets of synthetic graphs representing brains at different stages of neural maturation, and gain insights into developmental changes in their topological organization.

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Alterations in fMRI-based brain functional network connectivity (FNC) are associated with schizophrenia (SCZ) and the genetic risk or subthreshold clinical symptoms preceding the onset of SCZ, which often occurs in early adulthood. Thus, age-sensitive FNC changes may be relevant to SCZ risk-related FNC. We used independent component analysis to estimate FNC from childhood to adulthood in 9,236 individuals. To capture individual brain features more accurately than single-session fMRI, we studied an average of three fMRI scans per individual. To identify potential familial risk-related FNC changes, we compared age-related FNC in first-degree relatives of SCZ patients mostly including unaffected siblings (SIB) with neurotypical controls (NC) at the same age stage. Then, we examined how polygenic risk scores for SCZ influenced risk-related FNC patterns. Finally, we investigated the same risk-related FNC patterns in adult SCZ patients (oSCZ) and young individuals with subclinical psychotic symptoms (PSY). Age-sensitive risk-related FNC patterns emerge during adolescence and early adulthood, but not before. Young SIB always followed older NC patterns, with decreased FNC in a cerebellar-occipitoparietal circuit and increased FNC in two prefrontal-sensorimotor circuits when compared to young NC. Two of these FNC alterations were also found in oSCZ, with one exhibiting reversed pattern. All were linked to polygenic risk for SCZ in unrelated individuals (R varied from 0.02 to 0.05). Young PSY showed FNC alterations in the same direction as SIB when compared to NC. These results suggest that age-related neurotypical FNC correlates with genetic risk for SCZ and is detectable with MRI in young participants.

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As we move toward population-level developmental neuroscience, understanding intra- and inter-individual variability in brain maturation and sources of neurodevelopmental heterogeneity becomes paramount. Large-scale, longitudinal neuroimaging studies have uncovered group-level neurodevelopmental trajectories, and while recent work has begun to untangle intra- and inter-individual differences, they remain largely unclear. Here, we aim to quantify both intra- and inter-individual variability across facets of neurodevelopment across early adolescence (ages 8.92 to 13.83 years) in the Adolescent Brain Cognitive Development (ABCD) Study and examine inter-individual variability as a function of age, sex, and puberty. Our results provide novel insight into differences in annualized percent change in macrostructure, microstructure, and functional brain development from ages 9-13 years old. These findings reveal moderate age-related intra-individual change, but age-related differences in inter-individual variability only in a few measures of cortical macro- and microstructure development. Greater inter-individual variability in brain development were seen in mid-pubertal individuals, except for a few aspects of white matter development that were more variable between prepubertal individuals in some tracts. Although both sexes contributed to inter-individual differences in macrostructure and functional development in a few regions of the brain, we found limited support for hypotheses regarding greater male-than-female variability. This work highlights pockets of individual variability across facets of early adolescent brain development, while also highlighting regional differences in heterogeneity to facilitate future investigations in quantifying and probing nuances in normative development, and deviations therefrom.

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Many studies of brain-behavior relationships rely on univariate approaches where each variable of interest is tested independently, which does not allow for the simultaneous investigation of multiple correlated variables. Alternatively, multivariate approaches allow for examining relationships between psychopathology and neural substrates simultaneously. There are multiple multivariate methods to choose from that each have assumptions which can affect the results; however, many studies employ one method without a clear justification for its selection. Additionally, there are few studies illustrating how differences between methods manifest in examining brain-behavior relationships. The purpose of this study was to exemplify how the choice of multivariate approach can change brain-behavior interpretations.

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Research among adults reveals robust associations between discrimination and suicidality. However, the relationship between discrimination and suicidality is understudied in youth. Participants in the Adolescent Brain Cognitive Development study (n = 10  312) completed a measure of discrimination based on multiple attributes. The Kiddie Schedule for Affective Disorders and Schizophrenia was administered 1 year later to assess depressive disorders and suicidality (ideation and behavior). Logistic regressions, adjusting for age, sex, race/ethnicity, family income, lifetime depressive disorders, and body composition were conducted. Adjusting for covariates, discrimination based on weight (OR: 2.19), race/ethnicity/color (OR: 3.21), and sexual orientation (OR: 3.83) were associated with greater odds of reporting suicidality 1 year later (ps < 0.025). Nationality-based discrimination was not significantly associated with suicidality. Compared with those reporting no discrimination, youths reporting discrimination based on 2 or more attributes had nearly 5 times greater odds of recent suicidality (OR: 4.72; P < .001). The current study highlights the deleterious impacts of discrimination on mental health among youths reporting multiple forms of discrimination.

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Eating disorders often emerge during adolescence, and affected individuals frequently demonstrate high rates of psychiatric comorbidity, particularly with depressive and anxiety disorders. Although risk for eating disorders reflects both genetic and neurobiological factors, knowledge of how genetic risk for eating disorders relates to neurobiology and psychiatric symptoms during critical developmental periods remains limited. Here we simultaneously estimated associations between genetic risk, brain structure, and eating-disorder-related psychopathology symptoms in over 4,900 adolescents of European ancestry from the ABCD study (mean age (s.d.) = 9.94 (0.62) years). Polygenic scores for anorexia nervosa (AN PGS) and body mass index (BMI PGS) were related to three morphometric brain features—cortical thickness, surface area, and subcortical gray matter volume—and to latent psychopathology factors using structural equation modeling. We identified a three-factor structure of eating-disorder-related psychopathology symptoms: eating, distress, and fear factors. Increased BMI PGS were uniquely associated with greater eating factor scores. Moreover, greater BMI PGS predicted widespread increases in cortical thickness and reductions in surface area while AN PGS were related to reduced caudate volume. Altered default mode and visual network thickness was associated with greater eating factor scores, whereas distress and fear factor scores reflected a shared reduction in somatomotor network thickness. Our novel findings indicate that greater genetic risk for high BMI and altered cortical thickness of canonical brain networks underpin eating disorder symptomatology in early adolescence. As neurobiological factors appear to shape disordered eating earlier in development than previously thought, these results underscore the need for early detection and intervention efforts for eating disorders.

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Deficits in effective executive function, including inhibitory control are associated with risk for a number of psychiatric disorders and significantly impact everyday functioning. These complex traits have been proposed to serve as endophenotypes, however, their genetic architecture is not yet well understood. To identify the common genetic variation associated with inhibitory control in the general population we performed the first trans-ancestry genome wide association study (GWAS) combining data across 8 sites and four ancestries (N = 14,877) using cognitive traits derived from the stop-signal task, namely – go reaction time (GoRT), go reaction time variability (GoRT SD) and stop signal reaction time (SSRT). Although we did not identify genome wide significant associations for any of the three traits, GoRT SD and SSRT demonstrated significant and similar SNP heritability of 8.2%, indicative of an influence of genetic factors. Power analyses demonstrated that the number of common causal variants contributing to the heritability of these phenotypes is relatively high and larger sample sizes are necessary to robustly identify associations. In Europeans, the polygenic risk for ADHD was significantly associated with GoRT SD and the polygenic risk for schizophrenia was associated with GoRT, while in East Asians polygenic risk for schizophrenia was associated with SSRT. These results support the potential of executive function measures as endophenotypes of neuropsychiatric disorders. Together these findings provide the first evidence indicating the influence of common genetic variation in the genetic architecture of inhibitory control quantified using objective behavioural traits derived from the stop-signal task.

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Delineating associations between images and covariates is a central aim of imaging studies. To tackle this problem, we propose a novel non-parametric approach in the framework of spatially varying coefficient models, where the spatially varying functions are estimated through deep neural networks. Our method incorporates spatial smoothness, handles subject heterogeneity, and provides straightforward interpretations. It is also highly flexible and accurate, making it ideal for capturing complex association patterns. We establish estimation and selection consistency and derive asymptotic error bounds. We demonstrate the method’s advantages through intensive simulations and analyses of two functional magnetic resonance imaging data sets.

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Only 16.1% percent of U.S. adolescents meet the recommendation of at least 60 minutes of moderate-to-vigorous intensity physical activity (MVPA) per day. Studies report declined levels of adolescent MVPA in early stages of the pandemic, but gaps remain in understanding changes beyond the initial three months of the pandemic. This study aims to describe and compare self-reported adolescent MVPA levels at multiple timepoints before and during the COVID-19 pandemic among 11,865 9-11-year-old U.S. adolescents from the Adolescent Brain Cognitive Development (ABCD) Study, including pre-pandemic (September 2016-October 2018), early (May, June, and August 2020), and later (October and December 2020, March 2021) stages of the pandemic. Poisson regression models with robust error variance were used to estimate crude and adjusted prevalence ratios (APRs) of the proportion of adolescents meeting national MVPA guidelines during early and later stages of the pandemic compared to pre-pandemic. The proportion of adolescents meeting MVPA guidelines decreased from pre (16.4%), early (11.0%), and later (4.7%) COVID-19 pandemic timepoints. Adolescent MVPA guideline adherence at early- and later-pandemic stages was 24% lower (APR 0.76, 95% CI 0.62, 0.93) and 68% lower (APR 0.32, 95% CI 0.24, 0.43) than pre-pandemic adherence, respectively. Weekly MVPA duration decreased throughout May 2020 to March 2021 (χ = 488.9, p < 0.0001). Study findings build upon existing evidence that the low achievement of national MVPA guidelines before the pandemic became even lower during the pandemic, demonstrating the need to support and improve access to adolescent MVPA opportunities during COVID-19 pandemic recovery efforts and in future pandemics.

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Neuroimaging-based prediction methods for intelligence have seen a rapid development. Among different neuroimaging modalities, prediction using functional connectivity (FC) has shown great promise. Most literature has focused on prediction using static FC, with limited investigations on the merits of such analysis compared to prediction using dynamic FC or region-level functional magnetic resonance imaging (fMRI) times series that encode temporal variability. To account for the temporal dynamics in fMRI, we propose a bi-directional long short-term memory (bi-LSTM) approach that incorporates feature selection mechanism. The proposed pipeline is implemented via an efficient algorithm and applied for predicting intelligence using region-level time series and dynamic FC. We compare the prediction performance using different fMRI features acquired from the Adolescent Brain Cognitive Development (ABCD) study involving nearly 7000 individuals. Our detailed analysis illustrates the consistently inferior performance of static FC compared to region-level time series or dynamic FC for single and combined rest and task fMRI experiments. The joint analysis of task and rest fMRI leads to improved intelligence prediction under all models compared to using fMRI from only one experiment. In addition, the proposed bi-LSTM pipeline based on region-level time series identifies several shared and differential important brain regions across fMRI experiments that drive intelligence prediction. A test-retest analysis of the selected regions shows strong reliability across cross-validation folds. Given the large sample size of ABCD study, our results provide strong evidence that superior prediction of intelligence can be achieved by accounting for temporal variations in fMRI.

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Multiple forms of parental psychopathology have been associated with differences in subcortical brain volume. However, few studies have considered the role of comorbidity. Here, we examine if alterations in child subcortical brain structure are specific to parental depression, anxiety, mania, or alcohol/substance use parental psychopathology, common across these disorders, or altered by a history of multiple disorders. We examined 6581 children aged 9 to 10 years old from the ABCD study with no history of mental disorders. We found several significant interactions such that the effects of a parental history of depression, anxiety, and substance use problems on amygdala and striatal volumes were moderated by comorbid parental history of another disorder. Interactions tended to suggest smaller volumes in the presence of a comorbid disorder. However, effect sizes were small, and no associations remained significant after correcting for multiple comparisons. Results suggest that associations between familial risk for psychopathology and offspring brain structure in 9-10-year-olds are modest, and relationships that do exist tend to implicate the amygdala and striatal regions and are moderated by a comorbid parental psychopathology history. Several methodological factors, including controlling for intracranial volume and other forms of parental psychopathology and excluding child psychopathology, likely contribute to inconsistencies in the literature.

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Structural similarity is a growing focus for magnetic resonance imaging (MRI) of connectomes. Here we propose Morphometric INverse Divergence (MIND), a new method to estimate within-subject similarity between cortical areas based on the divergence between their multivariate distributions of multiple MRI features. Compared to the prior approach of morphometric similarity networks (MSNs) on n > 11,000 scans spanning three human datasets and one macaque dataset, MIND networks were more reliable, more consistent with cortical cytoarchitectonics and symmetry and more correlated with tract-tracing measures of axonal connectivity. MIND networks derived from human T1-weighted MRI were more sensitive to age-related changes than MSNs or networks derived by tractography of diffusion-weighted MRI. Gene co-expression between cortical areas was more strongly coupled to MIND networks than to MSNs or tractography. MIND network phenotypes were also more heritable, especially edges between structurally differentiated areas. MIND network analysis provides a biologically validated lens for cortical connectomics using readily available MRI data.

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To evaluate whether prenatal tobacco exposure (PTE) is related to poorer cognitive performance, abnormal brain morphometry, and whether poor cognitive performance is mediated by PTE-related structural brain differences.

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Childhood overweight/obesity has been associated with negative consequences related to brain function and may involve alterations in white matter pathways important for cognitive and emotional processing. Aerobic physical activity is a promising lifestyle factor that could restore white matter alterations. However, little is known about either regional white matter alterations in children with overweight/obesity or the effects of aerobic physical activity targeting the obesity-related brain alterations in children. Using a large-scale cross-sectional population-based dataset of US children aged 9 to 10 years (n = 8019), this study explored the associations between overweight/obesity and microstructure of limbic white matter tracts, and examined whether aerobic physical activity may reduce the overweight/obesity-related white matter alterations in children. The primary outcome measure was restriction spectrum imaging (RSI)-derived white matter microstructural integrity measures. The number of days in a week that children engaged in aerobic physical activity for at least 60 minutes per day was assessed. We found that females with overweight/obesity had lower measures of integrity of the fimbria-fornix, a major limbic-hippocampal white matter tract, than their lean peers, while this difference was not significant in males. We also found a positive relationship between the number of days of aerobic physical activity completed in a week and integrity measures of the fimbria-fornix in females with overweight/obesity. Our results provide cross-sectional evidence of sex-specific microstructural alteration in the fimbria-fornix in children with overweight/obesity and suggest that aerobic physical activity may play a role in reducing this alteration. Future work should examine the causal direction of the relationship between childhood overweight/obesity and brain alterations and evaluate potential interventions to validate the effects of aerobic physical activity on this relationship.

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Physical symptoms, also known as somatic symptoms, are those for which medical examinations do not reveal a sufficient underlying root cause (e.g., pain and fatigue). The extant literature of the neurobiological underpinnings of physical symptoms is largely inconsistent and primarily comprises of (clinical) case-control studies with small sample sizes. In this cross-sectional study, we studied the association between dimensionally measured physical symptoms and brain morphology in pre-adolescents from two population-based cohorts; the Generation R Study (n = 2649, 10.1 ± 0.6 years old) and ABCD Study (n = 9637, 9.9 ± 0.6 years old). Physical symptoms were evaluated using continuous scores from the somatic complaints syndrome scale from the parent-reported Child Behavior Checklist (CBCL). High-resolution structural magnetic resonance imaging (MRI) was collected using 3-Tesla MRI systems. Linear regression models were fitted for global brain metrics (cortical and subcortical grey matter and total white matter volume) and surface-based vertex-wise measures (surface area and cortical thickness). Results were meta-analysed. Symptoms of anxiety/depression were studied as a contrasting comorbidity. In the meta-analyses across cohorts, we found negative associations between physical symptoms and surface area in the (i) left hemisphere; in the lateral orbitofrontal cortex and pars triangularis and (ii) right hemisphere; in the pars triangularis, the pars orbitalis, insula, middle temporal gyrus and caudal anterior cingulate cortex. However, only a subset of regions (left lateral orbitofrontal cortex and right pars triangularis) were specifically associated with physical symptoms, while others were also related to symptoms of anxiety/depression. No significant associations were observed for cortical thickness. This study in preadolescents, the most representative and well-powered to date, showed that more physical symptoms are modestly related to less surface area of the prefrontal cortex mostly. While these effects are subtle, future prospective research is warranted to understand the longitudinal relationship of physical symptoms and brain changes over time. Particularly, to elucidate whether physical symptoms are a potential cause or consequence of distinct neurodevelopmental trajectories.

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Screen time has been identified as a risk factor for childhood obesity, but the media landscape has evolved rapidly. Children with autism tend to be heavy users of screens and have an elevated prevalence of obesity. We know little about screen use patterns among children with autism vs. typically developing (TD) peers and in association with obesity.

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Adversity occurring during development is associated with detrimental health and quality of life outcomes, not just following exposure but throughout the lifespan. Despite increased research, there exists both overlapping and distinct definitions of early life adversity exposure captured by over 30 different empirically validated tools. A data-driven approach to defining and cataloging exposure is needed to better understand associated outcomes and advance the field.

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Childhood familiarity with (knowledge of) substances is a potentially important, currently understudied adolescent substance use risk factor. We aimed to describe changes in childhood familiarity with substances and to test whether baseline familiarity predicts early adolescent substance use.

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Childhood concussion may interfere with neurodevelopment and influence cognition. Females are more likely to experience persistent symptoms after concussion, yet the sex-specific impact of concussion on brain microstructure in children is understudied. This study examined white matter and cortical microstructure, based on neurite density (ND) from diffusion-weighted MRI, in 9-to-10-year-old children in the Adolescent Brain Cognitive Development Study with (n = 336) and without (n = 7368) a history of concussion, and its relationship with cognitive performance. Multivariate regression was used to investigate relationships between ND and group, sex, and age in deep and superficial white matter, subcortical structures, and cortex. Partial least square correlation was performed to identify associations between ND and performance on NIH Toolbox tasks in children with concussion. All tissue types demonstrated higher ND with age, reflecting brain maturation. Group comparisons revealed higher ND in deep and superficial white matter in females with concussion. In female but not male children with concussion, there were significant associations between ND and performance on cognitive tests. These results demonstrate a greater long-term impact of childhood concussion on white matter microstructure in females compared to males that is associated with cognitive function. The increase in ND in females may reflect premature white matter maturation.

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Exposure to childhood trauma is associated with numerous adverse mental health consequences. Addressing important gaps in the existing research, the proposed study clarifies the longitudinal and bidirectional associations between childhood trauma and both negative and positive emotion-driven impulsivity.

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Sexual minority (SM) youth experience a greater mental health burden compared with their heterosexual peers. This study aimed to characterize mental health disparities among SM compared with non-SM youth, test main and interactive associations of SM identity and stressors targeting SM youth at the individual level (interpersonal SM discrimination) and structural level (state-level structural SM stigma) with youth mental health, and explore the contribution of interpersonal SM discrimination to the mental health burden of SM youth.

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Chronic pain has economic costs on par with cardiovascular disease, diabetes, and cancer. Despite this impact on the health care system and an increasing awareness of the relationship between pain and mortality, efforts to identify simple symptom-based risk factors for the development of pain, particularly in children, have fallen short. This is critically important as pain that manifests during childhood often persists into adulthood. To date no longitudinal studies have examined symptoms in pain-free children that presage a new, multisite manifestation of pain in the future. We hypothesized that female sex, sleep problems and heightened somatic complaints at baseline would be associated with the risk of developing new multisite pain one year later.

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Childhood obesity is a major public health issue and is disproportionately prevalent among children from minority racial and ethnic groups. Personally mediated racism (commonly referred to as racial discrimination) is a known stressor that has been linked to higher body mass index (BMI; calculated as weight in kilograms divided by height in meters squared) in adults, but little is known about the association of racial discrimination and childhood and adolescent adiposity.

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Close friendships are important for mental health and cognition in late childhood. However, whether the more close friends the better, and the underlying neurobiological mechanisms are unknown. Using the Adolescent Brain Cognitive Developmental study, we identified nonlinear associations between the number of close friends, mental health, cognition, and brain structure. Although few close friends were associated with poor mental health, low cognitive functions, and small areas of the social brain (e.g., the orbitofrontal cortex, the anterior cingulate cortex, the anterior insula, and the temporoparietal junction), increasing the number of close friends beyond a level (around 5) was no longer associated with better mental health and larger cortical areas, and was even related to lower cognition. In children having no more than five close friends, the cortical areas related to the number of close friends revealed correlations with the density of μ-opioid receptors and the expression of OPRM1 and OPRK1 genes, and could partly mediate the association between the number of close friends, attention-deficit/hyperactivity disorder (ADHD) symptoms, and crystalized intelligence. Longitudinal analyses showed that both too few and too many close friends at baseline were associated with more ADHD symptoms and lower crystalized intelligence 2 y later. Additionally, we found that friendship network size was nonlinearly associated with well-being and academic performance in an independent social network dataset of middle-school students. These findings challenge the traditional idea of ‘the more, the better,’ and provide insights into potential brain and molecular mechanisms.

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To examine the prevalence, incidence, and transitions of suicide ideation and attempts and sex and racial/ethnic differences among children enrolled in three yearly assessments of the Adolescent Brain Cognitive Development Study. The forms of suicidal ideation (SI) (no SI, passive, nonspecific active, and active) among those who attempted suicide were also described.

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The transition from childhood to adolescence is characterized by enhanced neural plasticity and a consequent susceptibility to both beneficial and adverse aspects of one’s milieu.

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Maternal stress (MS) is a well-documented risk factor for impaired emotional development in offspring. Rodent models implicate the dentate gyrus (DG) of the hippocampus in the effects of MS on offspring depressive-like behaviors, but mechanisms in humans remain unclear. Here, we tested whether MS was associated with depressive symptoms and DG micro- and macrostructural alterations in offspring across 2 independent cohorts.

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Childhood is a crucial neurodevelopmental period. We investigated whether childhood reading for pleasure (RfP) was related to young adolescent assessments of cognition, mental health, and brain structure.

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Prediction of mental disorders based on neuroimaging is an emerging area of research with promising first results in adults. However, research on the unique demographic of children is underrepresented and it is doubtful whether findings obtained on adults can be transferred to children.

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Preterm birth is a global health problem and associated with increased risk of long-term developmental impairments, but findings on the adverse outcomes of prematurity have been inconsistent.

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Childhood attention-deficit/hyperactivity disorder (ADHD) symptoms are believed to result from disrupted neurocognitive development. However, evidence for the clinical and predictive value of neurocognitive assessments in this context has been mixed, and there have been no large-scale efforts to quantify their potential for use in generalizable models that predict individuals’ ADHD symptoms in new data. Using data drawn from the Adolescent Brain Cognitive Development Study (ABCD), a consortium that recruited a diverse sample of over 10,000 youth (ages 9-10 at baseline) across 21 U.S. sites, we develop and test cross-validated machine learning models for predicting youths’ ADHD symptoms using neurocognitive abilities, demographics, and child and family characteristics. Models used baseline demographic and biometric measures, geocoded neighborhood data, youth reports of child and family characteristics, and neurocognitive tests to predict parent- and teacher-reported ADHD symptoms at the 1-year and 2-year follow-up time points. Predictive models explained 15-20% of the variance in 1-year ADHD symptoms for ABCD Study sites that were left out of the model-fitting process and 12-13% of the variance in 2-year ADHD symptoms. Models displayed high generalizability across study sites and trivial loss of predictive power when transferred from training data to left-out data. Features from multiple domains contributed meaningfully to prediction, including neurocognition, sex, self-reported impulsivity, parental monitoring, and screen time. This work quantifies the information value of neurocognitive abilities and other child characteristics for predicting ADHD symptoms and provides a foundational method for predicting individual youths’ symptoms in new data across contexts.

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Sociodemographic disparities in adolescent physical activity have been documented but mostly rely on self-reported data. Our objective was to examine differences in device-based step metrics, including daily step count (steps d), by sociodemographic factors among a diverse sample of 10-to-14-year-old adolescents in the US.

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Associations between psychiatric problems and white matter (WM) microstructure have been reported in youth. Yet, a deeper understanding of this relation has been hampered by a dearth of well-powered longitudinal studies and a lack of explicit examination of the bidirectional associations between brain and behavior. We investigated the temporal directionality of WM microstructure and psychiatric symptom associations in youth.

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Problematic screen use, defined as an inability to control use despite private, social, and professional life consequences, is increasingly common among adolescents and can have significant mental and physical health consequences. Adverse Childhood Experiences (ACEs) are important risk factors in the development of addictive behaviors and may play an important role in the development of problematic screen use.

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Salivary bioscience has found increased utilization within pediatric research, given the non-invasive nature of self-collecting saliva for measuring biological markers. With this growth in pediatric utility, more understanding is needed of how social-contextual factors, such as socioeconomic factors or status (SES), influence salivary bioscience in large multi-site studies. Socioeconomic factors have been shown to influence non-salivary analyte levels across childhood and adolescent development. However, less is understood about relationships between these socioeconomic factors and salivary collection methodological variables (e.g., time of saliva collection from waking, time of day of saliva collection, physical activity prior to saliva collection, and caffeine intake prior to saliva collection). Variability in salivary methodological variables between participants may impact the levels of analytes measured in a salivary sample, thus serving as a potential mechanism for non-random systematic biases in analytes.

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Sex differences in pain become apparent during puberty. However, the influence of key pubertal characteristics and pubertal hormones on pain is largely unknown. We examined the prospective associations between self-reported and hormone-indicated pubertal characteristics and pain incidence and severity in 10- to 11-year-old pain-free youth in the Adolescent Brain Cognitive Development (ABCD) Study over 1 year. Puberty was measured at baseline and follow-up with self-report (Pubertal Development Scale [PDS]) and hormonal assessment (salivary dehydroepiandrosterone [DHEA], testosterone, and estradiol). Pain status (yes/no), intensity, and interference (0-10 numerical rating scale) in the past month were self-reported at follow-up. Pubertal maturity, progression, and asynchrony were examined in relation to pain onset and severity through confounder-adjusted generalized estimating equations modified Poisson and linear mixed regression models. Among 6631 pain-free youth at baseline, 1-year incident pain was 30.7%. In both sexes, higher PDS scores were associated with greater risk of pain onset (relative risk [RR] = 1.10 to 1.27, Ps < 0.01). In boys, higher PDS item variance was associated with greater pain incidence (RR = 1.11, 95% CI, 1.03-1.20) and interference (beta = 0.40, 95% CI, 0.03-0.76); higher PDS overall and gonadal scores were associated with higher pain intensity (Ps < 0.05). Associations with hormones were seen in boys only, with each 10-fold higher testosterone levels associated with a 40% lower risk of pain incidence (95% CI, -55% to -22%) and 1.30-point lower (95% CI, -2.12 to -0.48) pain intensity, and higher DHEA levels were associated with lower pain intensity (P = 0.020). Relationships between pubertal development and pain in peripubertal adolescents are sex specific and puberty measurement specific and warrant further investigation.

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Youth with symptoms of emotion dysregulation are at risk for a multitude of psychiatric diagnoses later in life. However, few studies have focused on the underlying neurobiology of emotion dysregulation. This study assessed the bidirectional relationship between emotion dysregulation symptoms and brain morphology throughout childhood and adolescence.

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The correlations between genetic risk for Alzheimer’s disease (AD) with comprehensive brain regions at a regional scale are still not well understood. We aim to explore whether these associations vary across different age stages.

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While the neuroanatomical correlates of impulsivity in youths have been examined, there is little research on whether those correlates are consistent across childhood/adolescence. The current study uses data from the age 11/12 ( = 7,083) visit of the Adolescent Brain Cognitive Development Study to investigate the replicability of previous work (Owens et al., 2020) the neuroanatomical correlates of impulsive personality traits identified at age 9/10. Neuroanatomy was measured using structural and diffusion magnetic resonance imaging, and impulsive personality was measured using the UPPS-P Impulsive Behavior Scale. Replicability was quantified using three Open Science Collaboration replication criteria, intraclass correlations, and elastic net regression modeling to make predictions across timepoints. Replicability was highly variable among traits: The neuroanatomical correlates of positive urgency showed substantial similarity between ages 9/10 and 11/12, negative urgency and sensation seeking showed moderate similarity across ages, and (lack of) premeditation and perseverance showed substantial dissimilarity across ages. In all cases, effect sizes between impulsive traits and brain variables were small. These findings suggest that, even for studies with large sample sizes and the same participant pool, the replicability of brain-behavior correlations across a 2-year period cannot be assumed. This may be due to developmental changes across the two timepoints or false-positive/false-negative results at one or both timepoints. These results also highlight an array of neuroanatomical structures that may be important to impulsive personality traits across development from childhood into adolescence. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

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Approximately 10% of births are preterm [PTB; <37 weeks gestational age (GA)], which confers risk for cognitive, behavioral, and mental health challenges. Using the large and relatively diverse (i.e., designed to reflect sociodemographic variation in the United States population) Adolescent Brain Cognitive Development Study (ABCD Study), we characterized the impact of PTB on brain structure in middle-late childhood (9-10 years). The ABCD sample covers the GA spectrum, and the large sample size (∼11,500) permits consideration of how associations between PTB and brain structure are impacted by GA, sex, birthweight, and analytic choices such as controlling for total brain size. We found a pattern of relative cortical thinning in temporoparietal and dorsal prefrontal regions and thickening of medial prefrontal and occipital regions in PTB compared with children born full term (≥37 weeks GA). This pattern was apparent when controlling for mean thickness and when considering moderate (>32 and <37 weeks GA) and very PTB (≤32 weeks GA) separately, relative to full term birth. Surface area (SA) and subcortical volumes showed reductions in PTB children that were largely attenuated when controlling for brain size. Effects on cortical thickness (CT) and surface area were partially mediated by birthweight. Although boys are at increased risk for adverse outcomes following PTB, there was limited evidence of sex differences of PTB effects. Finally, cortical thickness effects estimated in a “discovery” sample ( = 7528) predicted GA in a holdout “replication” sample ( = 2139). Our findings help to clarify the effects of PTB on brain structure into late childhood across the GA spectrum.

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This study proposes a novel heterogeneous graph convolutional neural network (HGCNN) to handle complex brain fMRI data at regional and across-region levels. We introduce a generic formulation of spectral filters on heterogeneous graphs by introducing the – Hodge-Laplacian (HL) operator. In particular, we propose Laguerre polynomial approximations of HL spectral filters and prove that their spatial localization on graphs is related to the polynomial order. Furthermore, based on the bijection property of boundary operators on simplex graphs, we introduce a generic topological graph pooling (TGPool) method that can be used at any dimensional simplices. This study designs HL-node, HL-edge, and HL-HGCNN neural networks to learn signal representation at a graph node, edge levels, and both, respectively. Our experiments employ fMRI from the Adolescent Brain Cognitive Development (ABCD; n=7693) to predict general intelligence. Our results demonstrate the advantage of the HL-edge network over the HL-node network when functional brain connectivity is considered as features. The HL-HGCNN outperforms the state-of-the-art graph neural networks (GNNs) approaches, such as GAT, BrainGNN, dGCN, BrainNetCNN, and Hypergraph NN. The functional connectivity features learned from the HL-HGCNN are meaningful in interpreting neural circuits related to general intelligence.

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Research has demonstrated associations between pubertal development and brain maturation. However, existing studies have been limited by small samples, cross-sectional designs, and inconclusive findings regarding directionality of effects and sex differences. We examined the longitudinal temporal coupling of puberty status assessed using the Pubertal Development Scale (PDS) and magnetic resonance imaging (MRI)-based grey and white matter brain structure. Our sample consisted of 8896 children and adolescents at baseline (mean age = 9.9) and 6099 at follow-up (mean age = 11.9) from the Adolescent Brain and Cognitive Development (ABCD) Study cohort. Applying multigroup Bivariate Latent Change Score (BLCS) models, we found that baseline PDS predicted the rate of change in cortical thickness among females and rate of change in cortical surface area for both males and females. We also found a correlation between baseline PDS and surface area and co-occurring changes over time in males. Diffusion tensor imaging (DTI) analyses revealed correlated change between PDS and fractional anisotropy (FA) for both males and females, but no significant associations for mean diffusivity (MD). Our results suggest that pubertal status predicts cortical maturation, and that the strength of the associations differ between sex. Further research spanning the entire duration of puberty is needed to understand the extent and contribution of pubertal development on the youth brain.

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Attention deficit/hyperactivity disorder (ADHD) is usually conceptualized as a childhood-onset neurodevelopmental disorder, in which symptoms either decrease steadily into adulthood or remain stable. A recent study challenged this view, reporting that for most with ADHD, diagnostic status fluctuates with age. We ask if such a ‘fluctuating’ ADHD symptom trajectory subgroup is present in other population-based and clinic-based cohorts, centered on childhood and adolescence.

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Early adolescence is characterized by rapid changes in executive function and increased vulnerability to internalizing difficulties. The aim of this study was to explore whether internalizing symptoms are stable across early adolescence and to identify possible links with executive function. Using data from the Adolescent Brain and Cognitive Development Study (ABCD), we identified four dimensions of internalizing symptoms from item-level ratings on the Child Behavior Checklist at ages 10 ( = 10,841) and 12 ( = 5,846), with an invariant factor structure across time. These dimensions corresponded to anxiety, depression, withdrawal, and somatic problems. We then examined associations between these dimensions and three aspects of executive function at age 10 measured by the NIH Toolbox: inhibition, shifting and working memory. Worse shifting and inhibition at age 10 was associated with elevated symptoms of anxiety and withdrawal cross-sectionally, while poor inhibition was also uniquely associated with symptoms of depression. Longitudinal associations were more limited: Worse inhibition at age 10 predicted greater symptoms of withdrawal at age 12, while worse shifting predicted fewer symptoms of anxiety 2 years later. These findings suggest that poor executive function in early adolescence is associated with greater internalizing difficulties and poor inhibition may contribute to later social withdrawal.

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Alcohol use emerges during early adolescence and is strongly associated with individual and peer risky, delinquent, and rule breaking behaviors. Genetic predisposition for risky behavior contributes to individual rule breaking in adolescence and can also evoke peer rule breaking or lead youth to select into delinquent peer groups via gene-environment correlations (rGE), collectively increasing risk for alcohol use. Little research has examined whether genetic predisposition for risky behavior contributes to individual and peer rule breaking behavior in developmental pathways to alcohol use in early adolescence or in large diverse racial/ethnic populations. To address this, polygenic scores for risky behavior were considered predictors of individual rule breaking, peer rule breaking, and alcohol sips using data from the Adolescent Brain Cognitive Development (ABCD) study at age 11-12 and 12-13 in a cross-time cross-lagged model. This was examined separately in European American (EA; n = 5113; 47% female), African American (AA; n = 1159; 50% female), and Hispanic/Latinx (Latinx; n = 1624; 48% female) subgroups accounting for sociodemographic covariates and genetic ancestry principal components. Polygenic scores were positively associated with all constructs in EAs, with individual rule breaking at age 11-12 in AAs and Latinx, and with alcohol sips at age 11-12 in Latinx. Individual and peer rule breaking were associated with one another across time only in the EA subgroup. In all subgroups, peer rule breaking at 12-13 was associated with alcohol sips at 12-13. Results indicate that alcohol sips in early adolescence are associated with individual and peer rule breaking with rGE implicated in EAs.

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Functional impairments in cognition are frequently thought to be a feature of individuals with depression or anxiety. However, documented impairments are both broad and inconsistent, with little known about when they emerge, whether they are causes or effects of affective symptoms, or whether specific cognitive systems are implicated. Here, we show, in the adolescent ABCD cohort (N = 11,876), that attention dysregulation is a robust factor underlying wide-ranging cognitive task impairments seen in adolescents with moderate to severe anxiety or low mood. We stratified individuals high in DSM-oriented depression or anxiety symptomology, and low in attention deficit hyperactivity disorder (ADHD), as well as vice versa – demonstrating that those high in depression or anxiety dimensions but low in ADHD symptoms not only exhibited normal task performance across several commonly studied cognitive paradigms, but out-performed controls in several domains, as well as in those low in both dimensions. Similarly, we showed that there were no associations between psychopathological dimensions and performance on an extensive cognitive battery after controlling for attention dysregulation. Further, corroborating previous research, the co-occurrence of attention dysregulation was associated with a wide range of other adverse outcomes, psychopathological features, and executive functioning (EF) impairments. To assess how attention dysregulation relates to and generates diverse psychopathology, we performed confirmatory and exploratory network analysis with different analytic approaches using Gaussian Graphical Models and Directed Acyclic Graphs to examine interactions between ADHD, anxiety, low mood, oppositional defiant disorder (ODD), social relationships, and cognition. Confirmatory centrality analysis indicated that features of attention dysregulation were indeed central and robustly connected to a wide range of psychopathological traits across different categories, scales, and time points. Exploratory network analysis indicated potentially important bridging traits and socioenvironmental influences in the relationships between ADHD symptoms and mood/anxiety disorders. Trait perfectionism was uniquely associated with both better cognitive performance and broad psychopathological dimensions. This work suggests that attentional dysregulation may moderate the breadth of EF, fluid, and crystalized cognitive task outcomes seen in adolescents with anxiety and low mood, and may be central to disparate pathological features, and thus a target for attenuating wide-ranging negative developmental outcomes.

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Undergoing puberty ahead of peers (‘earlier pubertal timing’) is an important risk factor for mental health problems during early adolescence. The current study examined pathways between pubertal timing and mental health via connectivity of neural systems implicated in emotional reactivity and regulation (specifically corticolimbic connections) in 9- to 14-year-olds.

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Youth raised in stressful environments are at increased risk for developing impulsive traits, which are a robust precursor of problem behaviors. Sleep may mediate the link between stress and problem behaviors as it is both sensitive to stress and essential for neurocognitive development underlying behavioral control during adolescence. The default mode network (DMN) is a brain network implicated in stress regulation and sleep. Yet, it is poorly understood how individual differences in resting-state DMN moderate the effect of stressful environments on impulsivity via sleep problems.

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Lower neighborhood and household socioeconomic status (SES) are associated with negative health outcomes and altered brain structure in children. It is unclear whether such findings extend to white matter and via what mechanisms.

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Air pollution is linked to neurodevelopmental delays, but its association with longitudinal changes in brain network development has yet to be investigated. We aimed to characterize the effect of PM, O, and NO exposure at ages 9-10 years on changes in functional connectivity (FC) over a 2-year follow-up period, with a focus on the salience (SN), frontoparietal (FPN), and default-mode (DMN) brain networks as well as the amygdala and hippocampus given their importance in emotional and cognitive functioning.

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Sleep problems and psychopathology symptoms are highly comorbid and bidirectionally correlated across childhood and adolescence. Whether these associations are specific to discrete profiles of sleep problems and specific internalizing and externalizing phenomena is currently unclear.

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Cognitive impairment in depression is poorly understood. Family history of depression is a potentially useful risk marker for cognitive impairment, facilitating early identification and targeted intervention in those at highest risk, even if they do not themselves have depression. Several research cohorts have emerged recently that enable findings to be compared according to varying depths of family history phenotyping, in some cases also with genetic data, across the life span.

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To examine how youth and their caregivers’ mental health risk factors for suicide are associated with youth firearm access inside and outside the home.

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Adolescence, a developmental period characterized by significant changes in sleep, is associated with normative increases in impulsivity. While short sleep duration has been linked to elevated impulsivity, the neural mechanism underlying the relationship between short sleep duration and elevated impulsivity remains poorly understood.

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The fornix is a white matter bundle located in the center of the hippocampaldiencephalic limbic circuit that controls memory and executive functions, yet its genetic architectures and involvement in brain disorders remain largely unknown. We carried out a genome-wide association analysis of 30,832 UK Biobank individuals of the six fornix diffusion magnetic resonance imaging (dMRI) traits. The post-GWAS analysis allowed us to identify causal genetic variants in phenotypes at the single nucleotide polymorphisms (SNP), locus, and gene levels, as well as genetic overlap with brain health-related traits. We further generalized our GWAS in adolescent brain cognitive development (ABCD) cohort. The GWAS identified 63 independent significant variants within 20 genomic loci associated (P < 8.33 × 10) with the six fornix dMRI traits. Geminin coiled-coil domain containing (GMNC) and NUAK family SNF1-like kinase 1 (NUAK1) gene were highlighted, which were found in UKB and replicated in ABCD. The heritability of the six traits ranged from 10% to 27%. Gene mapping strategies identified 213 genes, where 11 were supported by all of four methods. Gene-based analyses revealed pathways relating to cell development and differentiation, with astrocytes found to be significantly enriched. Pleiotropy analyses with eight neurological and psychiatric disorders revealed shared variants, especially with schizophrenia under the conjFDR threshold of 0.05. These findings advance our understanding of the complex genetic architectures of fornix and their relevance in neurological and psychiatric disorders.

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Alcohol expectancies (AE) during early adolescence predict early alcohol use initiation and problem drinking both cross-sectionally and prospectively well into adulthood. Yet, our understanding of the sociocultural factors associated with AE during this development period remains limited. This study examines associations between AE and sociocultural factors across various domains (i.e., individual, family, peer, school, community, and culture) in a demographically diverse sample of 10- to 14-year-old youth in the Adolescent Brain Cognitive Development Study (ABCD Study).

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The COVID-19 pandemic led to significant disruptions in the lifestyle behaviors of adolescents; however, there is a paucity of data on objective changes in health indicators of adolescents such as blood pressure, hypertension, and weight. The aim of this study is to quantify differences in blood pressure and weight before and during the COVID-19 pandemic among a demographically diverse national sample of early adolescents. We analyzed cross-sectional data from 2018 to 2020, corresponding to the second follow-up year (Year 2) of the Adolescent Brain Cognitive Development (ABCD) Study. Among 4,065 early adolescents (mean age 12.00, 49.4% female, 55.5% white), 3.4% vs 6.4% of adolescents had hypertension pre-pandemic vs during the pandemic ( < 0.001). The pandemic was associated with a 4.65 percentile (95% CI 2.65, 6.66) higher diastolic blood pressure, and a 1.68 kg (95% CI 0.51, 2.85) higher weight when adjusting for covariates. The pandemic was associated with a 1.97 higher odds of hypertension (95% CI 1.33, 2.92) compared to pre-pandemic when adjusting for covariates. Future studies should explore mechanisms and longitudinal trends in blood pressure among adolescents as they return to pre-pandemic lifestyle behaviors.

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Childhood psychiatric symptoms are often diffuse but can coalesce into discrete mental illnesses during late adolescence. We leveraged polygenic scores (PGSs) to parse genomic risk for childhood symptoms and to uncover related neurodevelopmental mechanisms with transcriptomic and neuroimaging data. In independent samples (Adolescent Brain Cognitive Development, Generation R) a narrow cross-disorder neurodevelopmental PGS, reflecting risk for attention deficit hyperactivity disorder, autism, depression and Tourette syndrome, predicted psychiatric symptoms through early adolescence with greater sensitivity than broad cross-disorder PGSs reflecting shared risk across eight psychiatric disorders, the disorder-specific PGS individually or two other narrow cross-disorder (Compulsive, Mood-Psychotic) scores. Neurodevelopmental PGS-associated genes were preferentially expressed in the cerebellum, where their expression peaked prenatally. Further, lower gray matter volumes in cerebellum and functionally coupled cortical regions associated with psychiatric symptoms in mid-childhood. These findings demonstrate that the genetic underpinnings of pediatric psychiatric symptoms differ from those of adult illness, and implicate fetal cerebellar developmental processes that endure through childhood.

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Early-life adversity has profound consequences for youth neurodevelopment and adjustment; however, experiences of adversity are heterogeneous and interrelated in complex ways that can be difficult to operationalize and organize in developmental research. We sought to characterize the underlying dimensional structure of co-occurring adverse experiences among a subset of youth (ages 9-10) from the Adolescent Brain Cognitive Development (ABCD) Study (N = 7115), a community sample of youth in the United States. We identified 60 environmental and experiential variables that reflect adverse experiences. Exploratory factor analysis identified 10 robust dimensions of early-life adversity co-occurrence, corresponding to conceptual domains such as caregiver substance use and biological caregiver separation, caregiver psychopathology, caregiver lack of support, and socioeconomic disadvantage / neighborhood lack of safety. These dimensions demonstrated distinct associations with internalizing problems, externalizing problems, cognitive flexibility, and inhibitory control. Non-metric multidimensional scaling characterized qualitative similarity among the 10 identified dimensions. Results supported a nonlinear three-dimensional structure representing early-life adversity, including continuous gradients of “perspective”, “environmental uncertainty”, and “acts of omission/commission”. Our findings suggest that there are distinct dimensions of early-life adversity co-occurrence in the ABCD sample at baseline, and the resulting dimensions may have unique implications for neurodevelopment and youth behavior.

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During childhood, neural systems supporting high-level cognitive processes undergo periods of rapid growth and refinement, which rely on the successful coordination of activation across the brain. Some coordination occurs via cortical hubs-brain regions that coactivate with functional networks other than their own. Adult cortical hubs map into three distinct profiles, but less is known about hub categories during development, when critical improvement in cognition occurs. We identify four distinct hub categories in a large youth sample (n = 567, ages 8.5-17.2), each exhibiting more diverse connectivity profiles than adults. Youth hubs integrating control-sensory processing split into two distinct categories (visual control and auditory/motor control), whereas adult hubs unite under one. This split suggests a need for segregating sensory stimuli while functional networks are experiencing rapid development. Functional coactivation strength for youth control-processing hubs are associated with task performance, suggesting a specialized role in routing sensory information to and from the brain’s control system.

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Evaluate changes in early adolescent substance use from May 2020 to May 2021 during the coronavirus disease 2019 pandemic using data from a prospective nationwide cohort: the Adolescent Brain Cognitive Development Study.

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The results of recent surveys that show high levels of symptoms of anxiety and depression have generated widespread concern about the mental health of US youth. Although such increases and their causes require immediate action, these symptoms alone do not indicate an epidemic of mental disorders in the US because they do not reflect mental disorders that are characterized by protracted duration and educational or social impairment. Unfortunately, there are no recent comparable data on the full range of common mental disorders. (e.g., Anxiety, Attention Deficit Hyperactivity Disorder, Major Depression, etc.) in nationally representative samples of US youth to provide a baseline for the reported increased distress in recent surveys. Therefore, we must rely on indirect information derived from surveys of subsets of symptoms and behaviors or of restricted age groups, and web-based samples with unknown biases and limited generalizability. This editorial describes how the findings from a recent report of prevalence of mental disorders in 9-10-year-old youths from the ABCD study can contribute to the national profile of mental disorders in youth. We highlight the need to address the lack of systematic data on youth emotional and behavioral disorders in the US through concerted efforts to coordinate the multi-agency sources of data on youth mental health. This will require harmonization of sampling and methods, informed application of internet-based tools based on systematic sampling and non-probability sampling methods and promotion of efforts to bridge the gap between population-based research and interventions at both the societal and individual levels.

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Attention Deficit Hyperactivity Disorder (ADHD) is characterized by inattention, hyperactivity, and impulsivity; however, other executive function dysregulation is common, including inhibition and working memory. This study aims to identify CT differences based on executive function performance in individuals with and without ADHD.

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Family history of depression is a robust predictor of early-onset depression, which may confer risk through alterations in neural circuits that have been implicated in reward and emotional processing. These alterations may be evident in youths who are at familial risk for depression but who do not currently have depression. However, the identification of robust and replicable findings has been hindered by few studies and small sample sizes. In the current study, we sought to identify functional connectivity (FC) patterns associated with familial risk for depression.

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Neural activation during reward processing is thought to underlie critical behavioral changes that take place during the transition to adolescence (e.g., learning, risk-taking). Though literature on the neural basis of reward processing in adolescence is booming, important gaps remain. First, more information is needed regarding changes in functional neuroanatomy in early adolescence. Another gap is understanding whether sensitivity to different aspects of the incentive (e.g., magnitude and valence) changes during the transition into adolescence. We used fMRI from a large sample of preadolescent children to characterize neural responses to incentive valence vs. magnitude during anticipation and feedback, and their change over a period of two years.

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Parkinson’s disease (PD) is a late-onset and genetically complex neurodegenerative disorder. Here we sought to identify genes and molecular pathways underlying the associations between PD and the volume of ten brain structures measured through magnetic resonance imaging (MRI) scans. We leveraged genome-wide genetic data from several cohorts, including the International Parkinson’s Disease Genomics Consortium (IPDG), the UK Biobank, the Adolescent Brain Cognitive Development (ABCD) study, the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE), the Enhancing Neuroimaging Genetics through Meta-Analyses (ENIGMA), and 23andMe. We observed significant positive genetic correlations between PD and intracranial and subcortical brain volumes. Genome-wide association studies (GWAS) – pairwise analyses identified 210 genomic segments with shared aetiology between PD and at least one of these brain structures. Pathway enrichment results highlight potential links with chronic inflammation, the hypothalamic-pituitary-adrenal pathway, mitophagy, disrupted vesicle-trafficking, calcium-dependent, and autophagic pathways. Investigations for putative causal genetic effects suggest that a larger putamen volume could influence PD risk, independently of the potential causal genetic effects of intracranial volume (ICV) on PD. Our findings suggest that genetic variants influencing larger intracranial and subcortical brain volumes, possibly during earlier stages of life, influence the risk of developing PD later in life.

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Relationships with companion animals have been associated with higher levels of prosocial behavior and lower levels of socioemotional difficulties for children and adolescents. Companion animals may be supportive of developing prosocial behavior in youth through practice with positive social interactions and the development of empathy and reciprocity skills. The goal of this study was to use a person-centered approach to investigate if living with a pet (including pet species) is associated with profiles of adolescent peer social behaviors (i.e., prosocial, aggressive), and size of their peer network.

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Among adults and adolescents, weight-based discrimination is associated with disordered eating. However, these relationships remain understudied in children. Given that weight-based discrimination is commonly reported among youth, and that childhood is a crucial developmental period for the onset of disordered eating, the current study assessed prospective associations between weight-based discrimination and eating pathology among participants in the Adolescent Brain Cognitive Development Study. At the one-year visit, children indicated whether they had experienced discrimination due to their weight within the past year. Parents completed a computerized clinical interview to determine the presence of sub-or-full threshold eating disorders (AN, BN, and BED) among their children. At the two-year visit, children completed the same assessment. Height and fasting weight were obtained. Logistic regressions, adjusting for age, sex, race/ethnicity, family income, BMI%ile, and parent-reported presence of the respective eating disorder at one-year, were conducted to assess the associations between weight-based discrimination and eating pathology. Participants were 10,299 children who completed measures at both the one- and two-year visits (M at one-year: 10.92 ± 0.64, 47.6 % female, 45.9 % racial/ethnic minority). The presence of weight-based discrimination, reported by 5.6 % (n = 574) of children, was significantly associated with a greater likelihood of reporting AN, BN, and BED one-year later (ORs: 1.94-4.91). Findings suggest that weight-based discrimination may confer additional risk for the onset of disordered eating, above and beyond the contribution of body weight. Intersectional research is needed to examine the role of multiple forms of discrimination in relation to the development of eating pathology.

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Using baseline data ( = 9875) from the Adolescent Brain Cognitive Development (ABCD) Study examining children aged 9 to 10 years, the current analyses included: (1) exploratory factor analysis (EFA) and confirmatory factor analysis (CFA) of neurocognitive measures administered during baseline collection, and (2) linear regression analyses on the Child Behavior Checklist (CBCL), controlling for demographic and socioeconomic factors. The neurocognitive tasks measured episodic memory, executive function (EF; attention), language skills, processing speed, working memory, visuospatial ability, and reasoning. The CBCL included composite scores of parent-reported internalizing, externalizing, and stress-related behavior problems. The study reported here serves as an extension of prior research using a principal components analysis (PCA) of the ABCD baseline data. We propose an alternative solution using factor analysis. Analyses revealed a three-factor structure: verbal ability (VA), executive function/processing speed (EF/PS), and working memory/episodic memory (WM/EM). These factors were significantly correlated with the CBCL scores, albeit with small effect sizes. These findings provide a novel three-factor solution to the structure of cognitive abilities measured in the ABCD Study, offering new insights into the association between cognitive function and problem behaviors in early adolescence.

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