Research Publications

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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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.

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

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

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

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

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

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

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

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

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

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

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

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

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

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Our capacity to measure diverse aspects of human biology has developed rapidly in the past decades, but the rate at which these techniques have generated insights into the biological correlates of psychopathology has lagged far behind. The slow progress is partly due to the poor sensitivity, specificity and replicability of many findings in the literature, which have in turn been attributed to small effect sizes, small sample sizes and inadequate statistical power. A commonly proposed solution is to focus on large, consortia-sized samples. Yet it is abundantly clear that increasing sample sizes will have a limited impact unless a more fundamental issue is addressed: the precision with which target behavioral phenotypes are measured. Here, we discuss challenges, outline several ways forward and provide worked examples to demonstrate key problems and potential solutions. A precision phenotyping approach can enhance the discovery and replicability of associations between biology and psychopathology.

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To investigate the neural mechanisms underlying the association between poorer working memory performance and higher body mass index (BMI) in children. We employed structural-(sMRI) and functional magnetic resonance imaging (fMRI) with a 2-back working memory task to examine brain abnormalities and their associations with BMI and working memory performance in 232 children with overweight/obesity (OW/OB) and 244 normal weight children (NW) from the Adolescent Brain Cognitive Development dataset. OW/OB had lower working memory accuracy, which was associated with higher BMI. They showed smaller gray matter (GM) volumes in the left superior frontal gyrus (SFG_L), dorsal anterior cingulate cortex, medial orbital frontal cortex, and medial superior frontal gyrus, which were associated with lower working memory accuracy. During the working memory task, OW/OB relative to NW showed weaker activation in the left superior temporal pole, amygdala, insula, and bilateral caudate. In addition, caudate activation mediated the relationship between higher BMI and lower working memory accuracy. Higher BMI is associated with smaller GM volumes and weaker brain activation in regions involved with working memory. Task-related caudate dysfunction may account for lower working memory accuracy in children with higher BMI.

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Brain scans acquired across large, age-diverse cohorts have facilitated recent progress in establishing normative brain aging charts. Here, we ask the critical question of whether cross-sectional estimates of age-related brain trajectories resemble those directly measured from longitudinal data. We show that age-related brain changes inferred from cross-sectionally mapped brain charts can substantially underestimate actual changes measured longitudinally. We further find that brain aging trajectories vary markedly between individuals and are difficult to predict with population-level age trends estimated cross-sectionally. Prediction errors relate modestly to neuroimaging confounds and lifestyle factors. Our findings provide explicit evidence for the importance of longitudinal measurements in ascertaining brain development and aging trajectories.

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Findings in adults have shown that crystallized measures of intelligence, which are more culturally sensitive than fluid intelligence measures, have greater heritability; however, these results have not been found in children. The present study used data from 8,518 participants between 9 and 11 years old from the Adolescent Brain Cognitive Development (ABCD) Study. We found that polygenic predictors of intelligence test performance (based on genome-wide association meta-analyses of data from 269,867 individuals) and of educational attainment (based on data from 1.1 million individuals) predicted neurocognitive performance. We found that crystallized measures were more strongly associated with both polygenic predictors than were fluid measures. This mirrored heritability differences reported previously in adults and suggests similar associations in children. This may be consistent with a prominent role of gene-environment correlation in cognitive development measured by crystallized intelligence tests. Environmental and experiential mediators may represent malleable targets for improving cognitive outcomes.

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Previously, a study using a sample of the Adolescent Brain Cognitive Development (ABCD)® study from the earlier 1.0 release found differences in several resting state functional MRI (rsfMRI) brain connectivity measures associated with children reporting anhedonia. Here, we aim to reproduce, replicate, and extend the previous findings using data from the later ABCD study 4.0 release, which includes a significantly larger sample.

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Macrostructural characteristics, such as cost of living and state-level anti-poverty programs relate to the magnitude of socioeconomic disparities in brain development and mental health. In this study we leveraged data from the Adolescent Brain and Cognitive Development (ABCD) study from 10,633 9-11 year old youth (5115 female) across 17 states. Lower income was associated with smaller hippocampal volume and higher internalizing psychopathology. These associations were stronger in states with higher cost of living. However, in high cost of living states that provide more generous cash benefits for low-income families, socioeconomic disparities in hippocampal volume were reduced by 34%, such that the association of family income with hippocampal volume resembled that in the lowest cost of living states. We observed similar patterns for internalizing psychopathology. State-level anti-poverty programs and cost of living may be confounded with other factors related to neurodevelopment and mental health. However, the patterns were robust to controls for numerous state-level social, economic, and political characteristics. These findings suggest that state-level macrostructural characteristics, including the generosity of anti-poverty policies, are potentially relevant for addressing the relationship of low income with brain development and mental health.

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Neuroinflammation is both a consequence and driver of overfeeding and weight gain in rodent obesity models. Advances in magnetic resonance imaging (MRI) enable investigations of brain microstructure that suggests neuroinflammation in human obesity. To assess the convergent validity across MRI techniques and extend previous findings, we used diffusion basis spectrum imaging (DBSI) to characterize obesity-associated alterations in brain microstructure in 601 children (age 9-11 years) from the Adolescent Brain Cognitive Development Study. Compared with children with normal-weight, greater DBSI restricted fraction (RF), reflecting neuroinflammation-related cellularity, was seen in widespread white matter in children with overweight and obesity. Greater DBSI-RF in hypothalamus, caudate nucleus, putamen, and, in particular, nucleus accumbens, correlated with higher baseline body mass index and related anthropometrics. Comparable findings were seen in the striatum with a previously reported restriction spectrum imaging (RSI) model. Gain in waist circumference over 1 and 2 years related, at nominal significance, to greater baseline RSI-assessed restricted diffusion in nucleus accumbens and caudate nucleus, and DBSI-RF in hypothalamus, respectively. Here we demonstrate that childhood obesity is associated with microstructural alterations in white matter, hypothalamus, and striatum. Our results also support the reproducibility, across MRI methods, of findings of obesity-related putative neuroinflammation in children.

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Aside from widely known cardiovascular implications, higher weight in children may have negative associations with brain microstructure and neurodevelopment.

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Co-occurring physical and psychological symptoms during childhood and early adolescence may increase risk of symptom persistence into adulthood.

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Issues with classifying psychopathology using narrow diagnostic categories have prompted calls for the use of dimensional approaches. Yet questions remain about how closely dimensional approaches reflect the way symptoms cluster in individuals, whether known risk factors (e.g. preterm birth) produce distinct symptom phenotypes, and whether profiles reflecting symptom clusters are associated with neurocognitive factors. To identify distinct profiles of psychopathology, latent class analysis was applied to the syndrome scales of the parent-reported Child Behaviour Checklist for 11,381 9- and 10- year-olds from the Adolescent Brain Cognitive Development study. Four classes were identified, reflecting different profiles, to which children were assigned probabilistically; Class 1 (88.6%) reflected optimal functioning; Class 2 (7.1%), predominantly internalising; Class 3 (2.4%), predominantly externalising; and Class 4 (1.9%), universal difficulties. To investigate the presence of a possible preterm behavioural phenotype, the proportion of participants allocated to each class was cross-tabulated with gestational age category. No profile was specific to preterm birth. Finally, to assess the neurocognitive factors associated with class membership, elastic net regressions were conducted revealing a relatively distinct set of neurocognitive factors associated with each class. Findings support the use of large datasets to identify psychopathological profiles, explore phenotypes, and identify associated neurocognitive factors.

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Preterm birth (PTB) is associated with increased risk for unfavorable outcomes such as deficits in attentional control and related brain structure alterations. Crucially, PTB is more likely to occur within the context of poverty. The current study examined associations between PTB and inhibitory control (IC) implicated brain regions/tracts and task performance, as well as the moderating role of early life poverty on the relation between PTB and IC-implicated regions/tracts/task performance. 2,899 children from the ABCD study were sampled for this study. Mixed effects models examined the relation between PTB and subsequent IC performance as well as prefrontal gray matter volume, white matter fractional anisotropy (FA), and mean diffusivity (MD). Household income was examined as a moderator. PTB was significantly associated with less improvement in IC task performance over time and decreased FA in left uncinate fasciculus (UF) and cingulum bundle (CB). Early life poverty moderated the relation between PTB and both CB FA and UF MD.

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Integrating multiple neuroimaging modalities to identify clusters of individuals and then associating these clusters with psychopathology is a promising approach for understanding neurobiological mechanisms that underlie psychopathology and the extent to which these features are associated with clinical symptoms.

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Recently, several studies have investigated the neurodevelopment of psychiatric disorders using brain data acquired via structural magnetic resonance imaging (sMRI). These analyses have shown the potential of sMRI data to provide a relatively precise characterization of brain structural biomarkers. Despite these advances, a relatively unexplored question is how reliable and consistent a model is when assessing subjects from other independent datasets. In this study, we investigate the performance and generalizability of the same model architecture trained from distinct datasets comprising youths in diverse stages of neurodevelopment and with different mental health conditions. We employed models with the same 3D convolutional neural network (CNN) architecture to assess autism spectrum disorder (ASD), attention deficit hyperactivity disorder (ADHD), brain age, and a measure of dimensional psychopathology, the Child Behavior Checklist (CBCL) total score. The investigated datasets include the Autism Brain Imaging Data Exchange II (ABIDE-II, N = 580), Attention Deficit Hyperactivity Disorder (ADHD-200, N = 922), Brazilian High-Risk Cohort Study (BHRCS, N = 737), and Adolescent Brain Cognitive Development (ABCD, N = 11,031). Models’ performance and interpretability were assessed within each dataset (for diagnosis tasks) and inter-datasets (for age estimation). Despite the demographic and phenotypic differences of the subjects, all models presented significant estimations for age (p value < 0.001) within and between datasets. In addition, most models showed a moderate to high correlation in age estimation. The results, including the models’ brain regions of interest (ROI), were analyzed and discussed in light of the youth neurodevelopmental structural changes. Among other interesting discoveries, we found that less confounded training datasets produce models with higher generalization capacity.

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The aim of the study was to examine the association between prenatal exposure to maternal Hypertensive disorder during pregnancy (HDP) on brain structure and neurocognitive functioning (NCF) in singleton children aged between 9 and 10 years using the baseline wave of the Adolescent Brain and Cognitive Development (ABCD) Study. The ABCD Study interviewed each child (and their parents), measured NCF, and performed neuroimaging. Exposure to maternal high blood pressure (HBP) and preeclampsia or eclampsia (PE/EL) were extracted from the developmental history questionnaire. Differences in cortical thickness (CTh) and five cognitive abilities (two executive functions, working and episodic memory, processing speed, and two language abilities) between exposed and unexposed children were examined using generalized linear models. The mediating effects of CTh, birthweight, and BMI on the relationship between maternal HDP on NCF were also examined. A total of 584-children exposed to HBP, 387-children exposed to PE/EL, and 5,877 unexposed children were included in the analysis. Neither CTh nor NCF differed between the exposed and unexposed children with or without adjusting for the confounders including the child’s age, sex, race, education, and birth histories. The whole-brain CTh did not mediate the relationships between HDP and NCF. However, the relationship between HDP and most of the NCF was mediated by the child’s birthweight and BMI. Exposure to maternal HDP can affect their offspring’s later-life cognitive abilities via low birthweight and BMI during childhood. Prospective longitudinal studies, following up from infancy, are needed to further delineate the association of HDP on children’s cognitive abilities.

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Using baseline (ages 9-10) and two-year follow-up (ages 11-12) data from monozygotic and dizygotic twins enrolled in the longitudinal Adolescent Brain Cognitive Development Study, we investigated the genetic and environmental contributions to microstructure and volume of nine subcortical gray matter regions. Microstructure was assessed using diffusion MRI data analyzed using restriction spectrum imaging (RSI) and diffusion tensor imaging (DTI) models. The highest heritability estimates (estimate [95% confidence interval]) for microstructure were found using the RSI model in the pallidum (baseline: 0.859 [0.818, 0.889], follow-up: 0.835 [0.787, 0.871]), putamen (baseline: 0.859 [0.819, 0.889], follow-up: 0.874 [0.838, 0.902]), and thalamus (baseline: 0.855 [0.814, 0.887], follow-up: 0.819 [0.769, 0.857]). For volumes the corresponding regions were the caudate (baseline: 0.831 [0.688, 0.992], follow-up: 0.848 [0.701, 1.011]) and putamen (baseline: 0.906 [0.875, 0.914], follow-up: 0.906 [0.885, 0.923]). The subcortical regions displayed high genetic stability (rA = 0.743-1.000) across time and exhibited unique environmental correlations (rE = 0.194-0.610). Individual differences in both gray matter microstructure and volumes can be largely explained by additive genetic effects in this sample.

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Bullying victimization is associated with a doubled risk of attempting suicide in adulthood. Two longitudinal brain morphometry studies identified the fusiform gyrus and putamen as vulnerable to bullying. No study identified how neural alterations may mediate the effect of bullying on cognition. We assessed participants with caregiver-reported bullying (N = 323) and matched non-bullied controls (N = 322) from the Adolescent Brain Cognitive Development Study dataset to identify changes in brain morphometry associated with ongoing bullying victimization over two years and determine whether such alterations mediated the effect of bullying on cognition. Bullied children (38.7% girls, 47.7% racial minorities, 9.88 ± 0.62 years at baseline) had poorer cognitive performance (P < 0.05), larger right hippocampus (P = 0.036), left entorhinal cortex, left superior parietal cortex, and right fusiform gyrus volumes (all P < 0.05), as well as larger surface areas in multiple other frontal, parietal, and occipital cortices. Thinner cortices were also found in the left hemisphere, particularly in the left temporal lobe, and right frontal region (all P < 0.05). Importantly, larger surface area in the fusiform cortices partially suppressed (12-16%), and thinner precentral cortices partially mitigated, (7%) the effect of bullying on cognition (P < 0.05). These findings highlight the negative impact of prolonged bullying victimization on brain morphometry and cognition.

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During the preadolescent period, when the cerebral thickness, curvature, and myelin are constantly changing, the brain’s regionalization patterns underwent persistent development, contributing to the continuous improvements of various higher cognitive functions. Using a brain atlas to study the development of these functions has attracted much attention. However, the brains of children do not always have the same topological patterns as those of adults. Therefore, age-specific brain mapping is particularly important, serving as a basic and indispensable tool to study the normal development of children. In this study, we took advantage of longitudinal data to create the brain atlas specifically for preadolescent children. The resulting human Child Brainnetome Atlas, with 188 cortical and 36 subcortical subregions, provides a precise period-specific and cross-validated version of the brain atlas that is more appropriate for adoption in the preadolescent period. In addition, we compared and illustrated for regions with different topological patterns in the child and adult atlases, providing a topologically consistent reference for subsequent research studying child and adolescent development.

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The data release of Adolescent Brain Cognitive Development (ABCD) Study represents an extensive resource for investigating factors relating to child development and mental wellbeing. The genotype data of ABCD has been used extensively in the context of genetic analysis, including genome-wide association studies and polygenic score predictions. However, there are unique opportunities provided by ABCD genetic data that have not yet been fully tapped. The diverse genomic variability, the enriched relatedness among ABCD subsets, and the longitudinal design of the ABCD challenge researchers to perform novel analyses to gain deeper insight into human brain development. Genetic instruments derived from the ABCD genetic data, such as genetic principal components, can help to better control confounds beyond the context of genetic analyses. To facilitate the use genomic information in the ABCD for inference, we here detail the processing procedures, quality controls, general characteristics, and the corresponding resources in the ABCD genotype data of release 4.0.

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Recent studies proposed a general psychopathology factor underlying common comorbidities among psychiatric disorders. However, its neurobiological mechanisms and generalizability remain elusive. In this study, we used a large longitudinal neuroimaging cohort from adolescence to young adulthood (IMAGEN) to define a neuropsychopathological (NP) factor across externalizing and internalizing symptoms using multitask connectomes. We demonstrate that this NP factor might represent a unified, genetically determined, delayed development of the prefrontal cortex that further leads to poor executive function. We also show this NP factor to be reproducible in multiple developmental periods, from preadolescence to early adulthood, and generalizable to the resting-state connectome and clinical samples (the ADHD-200 Sample and the Stratify Project). In conclusion, we identify a reproducible and general neural basis underlying symptoms of multiple mental health disorders, bridging multidimensional evidence from behavioral, neuroimaging and genetic substrates. These findings may help to develop new therapeutic interventions for psychiatric comorbidities.

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