Scientific Publications

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During adolescence processes that control food intake (executive functions [EF]) undergo extensive refinement; underlying differences in EF may explain the inability to resist overeating unhealthy foods. Yet, overeating fat and sugar also causes changes to EF and cognition but disentangling these relationships has been difficult, as previous studies included youth with obesity. Here, amongst youth initially of a healthy weight, we evaluate whether 1) sex-specific underlying variation in EF/cognition at 9/10-years-old predict fat/sugar two-years later (Y2) and 2) if these relationships are moderated by body mass index (BMI), using linear mixed effects models (controlled for puberty, caregiver education; random effect: study site). Data were leveraged from Adolescent Brain Cognitive Development Study (n = 2987; 50.4% male; 15.4% Latino/a/x; 100% healthy weight at baseline; 12.4% overweight/obese by Y2, data release 4.0). EF and cognition (e.g., inhibition, impulsivity, cognition, motor, memory) were assessed with the NIH toolbox, Rey Auditory Verbal Listening Test, Little Man Task, the BIS/BAS, and UPPS-P. A saturated fat/added sugar (kcals) composite score was extracted from the validated Kids Food Block Screener. For males, greater baseline impulsivity (e.g., Positive Urgency, Lack of Planning and Perseverance) and reward (e.g., Fun seeking, Drive) was related to greater Y2 intake. For both sexes, greater baseline Negative Urgency and higher BMI was related to greater Y2 intake. No other relationships were observed. Our findings highlight a phenotype that may be more at risk for weight gain due to overconsumption of fat/sugar. Thus, prevention efforts may wish to focus on impulsive tendencies for these foods.

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Happiness is a fundamental human affective trait, but its biological basis is not well understood. Using a novel approach, we construct LDpred-inf polygenic scores of a general happiness measure in 2 cohorts: the Adolescent Brain Cognitive Development (ABCD) cohort (N = 15,924, age range 9.23-11.8 years), the Add Health cohort (N = 9129, age range 24.5-34.7) to determine associations with several well-being and happiness measures. Additionally, we investigated associations between genetic scores for happiness and brain structure in ABCD (N = 9626, age range (8.9-11) and UK Biobank (N = 16,957, age range 45-83). We detected significant (p.FDR < 0.05) associations between higher genetic scores vs. several well-being measures (best r = 0.019) in children of multiple ancestries in ABCD and small yet significant correlations with a happiness measure in European participants in Add Health (r = 0.004). Additionally, we show significant associations between lower genetic scores for happiness with smaller structural brain phenotypes in a white British subsample of UK Biobank and a white sub-sample group of ABCD. We demonstrate that the genetic basis for general happiness level appears to have a consistent effect on happiness and wellbeing measures throughout the lifespan, across multiple ancestral backgrounds, and multiple brain structures.

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The association between excessive screen media use and mental health problems has attracted widespread attention. The literature to date has neglected the biological mechanisms underlying such a relationship and failed to distinguish between different types of screen media activities. A sample from the Adolescent Brain and Cognitive Development study was used in the present study to elucidate the longitudinal associations between specific types of screen media use, brain development, and diverse mental health problems. The results showed that different types of screen media use have differentiated associations with mental health problems, subcortical volume, and cortical-subcortical connectivity. Specifically, more passive media use was associated with increased rule-breaking behavior, while more video game playing was associated with increased withdrawn/depressed symptoms. In addition, more social media use was associated with a reduced volume of the hippocampus, caudate, and thalamus proper. More research is needed to examine the differential effects of screen media use on neurodevelopmental processes and mental health problems across adolescence.

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Early life adversity is associated with differences in cognition and mental health that can impact on daily functioning. This study uses a hybrid machine-learning approach that combines random forest classification with hierarchical clustering to clarify whether there are cognitive differences between individuals who have experienced moderate-to-severe adversity relative to those have not experienced adversity, to explore whether different forms of adversity are associated with distinct cognitive alterations and whether these such alterations are related to mental health using data from the ABCD study ( = 5,955). Cognitive measures spanning language, reasoning, memory, risk-taking, affective control, and reward processing predicted whether a child had a history of adversity with reasonable accuracy (67%), and with good specificity and sensitivity (>70%). Two subgroups were identified within the adversity group and two within the no-adversity group that were distinguished by cognitive ability (low vs high). There was no evidence for specific associations between the type of adverse exposure and cognitive profile. Worse cognition predicted lower levels of mental health in unexposed children. However, while children who experience adversity had elevated mental health difficulties, their mental health did not differ as a function of cognitive ability, thus providing novel insight into the heterogeneity of psychiatric risk.

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Pubertal development has been separately linked to adolescents’ sleep problems and larger family functioning, but research connecting these inter-related processes remains sparse. This study aimed to examine how pubertal status and tempo were related to early adolescents’ sleep and their family functioning. Using longitudinal data from the Adolescent Brain and Cognitive Development study, the study’s sample (N = 4682) was 49.2% female, was an average of 9.94 years old at baseline, and was 60.1% white. Analyses in the current study modeled the indirect associations between pubertal change and changes in family conflict via adolescent sleep duration and variability of duration. The results suggested that pubertal status and tempo predicted shorter adolescent sleep durations and greater variability in those durations, which predicted residual increases in family conflict. The findings highlight the role of adolescents’ pubertal changes in their sleep and how such changes can negatively affect family functioning.

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The present study characterized sleep profiles in a national longitudinal sample of early adolescents and examined whether profiles predicted later behavioral problems.

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We aimed to identify significant contributing factors to the risk of maladaptive behaviors, such as alcohol use disorder or obesity, in children. To achieve this, we utilized the extensive adolescent brain cognitive development data set, which encompasses a wide range of environmental, social, and nutritional factors.

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Elevated levels of behavioral inhibition (BI) may connote risk for both anxiety and substance use disorders. BI has consistently been shown to be associated with increased levels of anxiety, while the association between BI and substance use has been mixed. It is possible that the relationship between BI and substance use varies by individual difference factors. Hispanic/Latinx (H/L) youth in particular may have stronger relationships between BI, anxiety, and substance use.

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Emerging evidence suggests an association between maternal hypertension during pregnancy and mental health in the offspring. However, less is known about the role of hypertensive pregnancy in behavioral symptoms and brain structures of the offspring as well as in their developmental changes. Here, we utilized neuroimaging and behavioral data from 11,878 participants aged 9-10 years and their 2-year follow-up from the Adolescent Brain Cognitive Development (ABCD) study to investigate the long-term effects of maternal hypertension during pregnancy on early adolescent behavior and brain anatomy. Specifically, adolescents born of mothers with maternal hypertension are at risk of long-lasting behavioral problems, as manifested by higher externalizing and internalizing behavior scores at both 9-10 years and 11-12 years. These participants additionally presented with a higher cortical thickness, particularly in the fronto-parieto-temporal areas at 9-10 years. Four regions, including the left parahippocampus, left lateral orbitofrontal lobe, right superior temporal lobe and right temporal pole, remained thicker 2 years later. These findings were partially validated in rats modeled with Nω-nitro-L-arginine methyl ester (L-NAME) preeclampsia. Therefore, clinicians and women who experience hypertension during pregnancy should be warned of this risk, and healthcare providers should recommend appropriate clinical interventions for pregnancy-induced hypertension.

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This study examined the independent and interactive effects of alcohol use disorder genome-wide polygenic scores (AUD-PGS) and parenting and family conflict on early adolescent externalizing behaviors. Data were drawn from White (N = 6181, 46.9% female), Black/African American (N = 1784, 50.1% female), and Hispanic/Latinx (N = 2410, 48.0% female) youth from the adolescent brain cognitive development Study (ABCD). Parents reported on youth externalizing behaviors at baseline (T1, age 9/10), 1-year (T2, age 10/11) and 2-year (T3, age 11/12) assessments. Youth reported on parenting and family environment at T1 and provided saliva or blood samples for genotyping. Results from latent growth models indicated that in general externalizing behaviors decreased from T1 to T3. Across all groups, higher family conflict was associated with more externalizing behaviors at T1, and we did not find significant associations between parental monitoring and early adolescent externalizing behaviors. Parental acceptance was associated with lower externalizing behaviors among White and Hispanic youth, but not among Black youth. Results indicated no significant main effect of AUD-PGS nor interaction effect between AUD-PGS and family variables on early adolescent externalizing behaviors. Post hoc exploratory analysis uncovered an interaction between AUD-PGS and parental acceptance such that AUD-PGS was positively associated with externalizing rule-breaking behaviors among Hispanic youth, but only when parental acceptance was very low. Findings highlight the important role of family conflict and parental acceptance in externalizing behaviors among early adolescents, and emphasize the need to examine other developmental pathways underlying genetic risk for AUD across diverse populations.

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Despite the known benefits of data-driven approaches, the lack of approaches for identifying functional neuroimaging patterns that capture both individual variations and inter-subject correspondence limits the clinical utility of rsfMRI and its application to single-subject analyses. Here, using rsfMRI data from over 100k individuals across private and public datasets, we identify replicable multi-spatial-scale canonical intrinsic connectivity network (ICN) templates via the use of multi-model-order independent component analysis (ICA). We also study the feasibility of estimating subject-specific ICNs via spatially constrained ICA. The results show that the subject-level ICN estimations vary as a function of the ICN itself, the data length, and the spatial resolution. In general, large-scale ICNs require less data to achieve specific levels of (within- and between-subject) spatial similarity with their templates. Importantly, increasing data length can reduce an ICN’s subject-level specificity, suggesting longer scans may not always be desirable. We also find a positive linear relationship between data length and spatial smoothness (possibly due to averaging over intrinsic dynamics), suggesting studies examining optimized data length should consider spatial smoothness. Finally, consistency in spatial similarity between ICNs estimated using the full data and subsets across different data lengths suggests lower within-subject spatial similarity in shorter data is not wholly defined by lower reliability in ICN estimates, but may be an indication of meaningful brain dynamics which average out as data length increases.

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Approximately half of adolescents encounter a mismatch between their sleep patterns on school days and free days, also referred to as “social jetlag”. This condition has been linked to various adverse outcomes, such as poor sleep, cognitive deficits, and mental disorders. However, prior research was unsuccessful in accounting for other variables that are correlated with social jetlag, including sleep duration and quality. To address this limitation, we applied a propensity score matching method on a sample of 6335 11-12-year-olds from the two-year follow-up (FL2) data of the Adolescent Brain Cognitive Development (ABCD) study. We identified 2424 pairs of participants with high sleep-corrected social jetlag (SJLsc, over 1 hour) and low SJLsc (<= 1 hour) at FL2 (1728 pairs have neuroimaging data), as well as 1626 pairs at three-year follow-up (FL3), after matching based on 11 covariates including socioeconomic status, demographics, and sleep duration and quality. Our results showed that high SJLsc, as measured by the Munich Chronotype Questionnaire, was linked to reduced crystallized intelligence, lower school performance – grades, and decreased functional connectivity between cortical networks and subcortical regions, specifically between cingulo-opercular network and right hippocampus. Further mediation and longitudinal mediation analyses revealed that this connection mediated the associations between SJLsc and crystallized intelligence at FL2, and between SJLsc and grades at both FL2 and FL3. We validated these findings by replicating these results using objective SJLsc measurements obtained via Fitbit watches. Overall, our study highlights the negative association between social jetlag and crystallized intelligence during early adolescence.

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Life history theory posits that multigenerational exposure to adversity and deprivation influences childhood growth and development, including pubertal maturation. We applied this ecological, evolutionary theory to examine the contributions of distal and proximal adversity on early puberty, a potentially important marker for population health.

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Introduction
Externalizing behaviors are defined as behaviors violating social norms and can be harmful to self and others. Predicting the escalation of externalizing behaviors in children would allow for early interventions to prevent the occurrence of antisocial and criminal acts. Externalizing behaviors are heritable traits, and have been associated with structures of the brain. Brain structure, in turn, is also influenced by genetics. Here, we investigated the association of genetic and brain structural variation with externalizing behaviors in late childhood, and we assessed potential mediating effects.

Methods
Data was collected for 11,878 children aged 9–10 years old from the Adolescent Brain Cognitive Development (ABCD) cohort. We extracted data on externalizing behaviors measured by the parent-reported Child Behavior Checklist (CBCL), brain volumes and white matter integrity measured by magnetic resonance imaging (MRI), and polygenic risk scores (PRS) for (i) antisocial behaviors, (ii) attention-deficit/hyperactivity disorder comorbid with disruptive behavior disorder (ADHD ​+ ​DBD), (iii) irritability, and (iv) traits related to self-regulation & addiction. We examined the associations between brain structures, PRS, and externalizing behavior, and to what extent brain structures mediate the association between PRS and externalizing behavior. Phenotypic associations between brain structures and externalizing behaviors were validated in an independent cohort of 150 adolescents aged 12–21 years enriched for individuals with antisocial behavior.

Results
Increasing levels of externalizing behaviors were associated with reduced total brain and focal gray matter volumes, but not with white matter integrity. These results could not be validated in the independent cohort, except for a good correlation of several effect sizes between the cohorts. Higher PRS for externalizing behaviors were associated with lower cortical gray matter volume, larger subcortical gray matter volume, larger white matter volume, and reduced global white matter fractional anisotropy. Genetic and brain structural variation, combined with sociodemographic factors, explained up to 7% of variation in externalizing behaviors in late childhood; brain structures and PRS each explained up to ∼0.5% of variation. A multivariate model with all sociodemographic factors, brain structures and PRS combined explained up to 11.9% (+5%). Total cortical gray matter volume mediated the association between PRS for ADHD ​+ ​DBD and externalizing behavior in late childhood. However, a large proportion of individual variation in externalizing behavior remained unidentified (∼90%). Brain function and interaction effects with the environment are surmised as potential sources of additional variation.

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Cannabis is the most used federally illicit substance among pregnant people in the United States. However, emerging preclinical data show that a significant portion of cannabis constituents, such as Δ-tetrahydrocannabinol and its bioactive metabolites, readily cross the placenta and accumulate in the fetal brain, disrupting neurodevelopment. Recent research using the Adolescent Brain Cognitive Development (ABCD) Study cohort has linked prenatal cannabis exposure (PCE) to greater neurobehavioral problems and lower total gray and white matter volume in children. Here, we examined the impact of PCE on frontolimbic white matter pathways that are critical for cognitive- and emotion-related functioning, show a high density of cannabinoid receptors, and are susceptible to cannabis exposure during other periods of rapid neurodevelopment (e.g., adolescence).

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Delay discounting is a well-established risk factor for risky behaviors and the development of externalizing spectrum disorders. Building upon recent work that developed a novel cortical marker of delay discounting (C-DD) in adult samples, the objective of this study was to test whether the C-DD relates to delay discounting and subsequently externalizing pathology in adolescent samples. The current study used two samples: 9992 early adolescents participating in the ABCD study (Mage = 9.93 years old, 48.7% female), and 56 early adolescents recruited from the community (Mage = 12.27 years old, 55.4% female). Cortical thickness was estimated using the FreeSurfer standard pipeline, and the cortical marker of delay discounting (C-DD) was calculated based on procedures outlined by the initial validation study. All data are cross-sectional in nature. As expected, C-DD was positively related to delay discounting in the ABCD sample, even after accounting for age, biological sex, collection site and data quality indicators. Moreover, results showed that C-DD was discriminately associated with externalizing, but not internalizing, symptoms in both samples of young adolescents. Findings replicate those found in adult samples, suggestive that C-DD may be a useful neuroanatomical marker of youth delay discounting. Replication of findings in other samples will be needed to determine whether C-DD has translational relevance to understanding externalizing psychopathology in adolescent samples.

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Effortful control, the ability to regulate complex and goal-directed behavior, may protect individuals from developing mental health symptoms. This study tested the potential for child effortful control and executive functioning to buffer the effects of familial liability for attention deficit hyperactivity disorder (ADHD) problems across a one-year timeframe. Data from the prospectively-collected Adolescent Brain Cognitive Development (ABCD)® study were used to examine whether caregiver-rated child effortful control and executive functioning moderated the association between familial ADHD risk and later ADHD symptoms in a sample of children (N = 6,133; ages 9-10 years at baseline). Two independent variables were considered to compare the predictive powers of specific (family ADHD) and broad (family psychopathology) risk factors. Two additional moderating variables (surgency, negative affect) were tested to examine specificity of effortful control and executive functioning as moderators. All variables of interest were measured on a continuum and via caregiver report. At high levels of effortful control and executive functioning, there was no association between familial liability for ADHD or broad psychopathology and later child ADHD problems. The moderator effects were specific to effortful control and executive functioning domains. Etiological models of heritable psychiatric disorders, such as ADHD, should consider the risk and protective contributions of individual traits, such as effortful control and executive functioning. Clinical prevention and intervention efforts may target self-regulation skills in children to buffer against familial liability for ADHD problems.

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Cognitive function and general psychopathology are two important classes of human behavior dimensions, individually relate to mental disorders across diagnostic categories. However, whether the two transdiagnostic dimensions link to common or distinct brain networks that convey resilience or risk for the development of psychiatric disorders remains unclear.

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Accurate psychiatric risk assessment requires biomarkers that are both stable and adaptable to development. Functional network connectivity (FNC), which steadily reconfigures over time, potentially contains abundant information to assess psychiatric risks. However, the absence of suitable analytical methodologies has constrained this area of investigation.

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To assess the relationship between adverse childhood experiences (ACEs) and objective measures of physical activity and sleep.

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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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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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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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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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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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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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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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