Research Publications

Abstract

Background & Aims
Adverse experiences during early life can disrupt gut-brain axis development, but the mechanisms linking early life stress (ELS) to long-term gastrointestinal (GI) dysmotility and pain remain unclear.

Methods
We used a maternal separation (MS) mouse model of ELS and assessed visceral pain sensitivity, intestinal motility, and enteric nervous system (ENS) composition. Two large human pediatric population cohorts were also analyzed for associations between early life stress and DGBI risk.

Results
MS in mice led to visceral hypersensitivity, sex-specific motility defects, and altered ENS composition, including increased serotonergic innervation and changes in subtype-specific neuronal proportions. Degarelix-mediated suppression of gonadal hormones reversed MS-induced visceral pain and motility defects, implicating sex hormones in long-term gut changes. MS led to enhanced sympathetic innervation of the ENS and chemical sympathectomy restored normal motility, suggesting sympathetic overactivity in ELS-related gut dysfunction. In humans, significant associations between maternal mental health problems and pediatric disorders of gut-brain interaction (DGBI) were observed in both cohorts, mirroring preclinical findings.

Conclusion
These results identify ELS-driven changes in enteric, sensory, and sympathetic pathways as contributors to DGBI risk and offer insight into potential therapeutic targets.

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Pediatric mild traumatic brain injury (mTBI) is a major public health concern. New psychiatric disorders (NPDs) can arise after mTBI, yet postinjury NPDs in nonclinical samples remain poorly understood.

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Introduction: Youth with diabetes are at a higher risk for mental health challenges. Despite this awareness, there is much to learn how factors of a child’s environment, such as pet ownership, may promote better diabetes-related health outcomes. This study assessed if pet ownership in diabetic youth was associated with anxiety/depression, parental stress, and A1C, as well as if geographic prevalence of diabetes differed by pet ownership status.

Methods: Data were obtained from the Adolescent Brain Cognitive Development (ABCD) Study, including participants with pet ownership data (n = 9,802). Primary analyses were conducted with a subsample of youth with diabetes (n = 80).

Results: There were no statistically significant relationships between pet ownership and anxiety/depression or parental stress. A1C levels among pet owners and non pet owners were explored (n = 10). In the full sample (n = 9,802), there was a significant difference between pet owners and non-pet owners on geographical diabetes prevalence where pet owners were more likely to live in communities with lower rates of diabetes.

Conclusions: Pet ownership was not associated with mental health in families with diabetes. Preliminary analyses indicated the potential for an association between A1C and pet ownership as well as geographic prevalence of diabetes and living with a pet.

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Objective
The current study aims to determine heterogenous latent profiles of substance use perceived harm and examine the concurrent associations between profiles and substance use experimentation.

Methods
We used data from the Adolescent Brain Cognitive DevelopmentSM Study (5.1 data release) 1-year follow up. Participants (N = 11184) were 52.2% male between the ages of 9 and 14 (Mage = 10.48, SD = 0.65). Latent profile analysis was used with 11 perceived harm indicators. Multinomial logistic regression was used to determine the association between profile membership and substance use experimentation (i.e., alcohol sipping, tobacco puffing, and cannabis puffing).

Results
A four-profile solution fit the data best. The four profiles included participants in 1) high harm perceptions across all substances, 2) low harm perceptions across all substances, 3) moderate harm perceptions across all substances, and 4) selective high-harm perceptions for some substances. Those in the low harm profile (AOR = 4.99, p <.01) and selective high-harm profile (AOR = 3.04, p <.05) were more likely to report puffing tobacco compared to the high harm profile. Also, those in the moderate harm profile (AOR = 1.36, p <.05) and those in the selective high-harm profile (AOR = 1.56, p <.001) were more likely to report sipping alcohol compared to the high harm group.

Conclusion
The four-profile solution illustrates meaningful heterogeneity in how youth perceive substance-related harm, suggesting the need for more tailored prevention approaches rather than one-size-fits-all messaging considering that even partial recognition of risk may not fully protect against experimenting with substances.

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Mild traumatic brain injury (mTBI) disproportionately affects children and adolescents and has been associated with poorer neurocognitive performance, but the biological mechanisms driving symptom variability and severity remain understudied. In accordance with the omnigenic disease model, we integrated gene-by-mTBI interaction genome-wide association studies on neurocognition from the Adolescent Brain Cognitive Development (ABCD) cohort with single-cell RNA sequencing gene regulatory networks to elucidate the cell type-specific key regulators and molecular mechanisms governing neurocognitive outcome of mTBI, specifically learning and memory performance. Our analysis revealed distinct network regulators in neuronal and glial cell types across hippocampal and cortical brain regions to orchestrate key neurodevelopmental pathways. Examples include APP for synaptic signaling in excitatory neurons, COX5A for mitochondrial function in inhibitory neurons, MOG for myelination in oligodendrocytes in the hippocampus; GRM7 for synaptic signaling in excitatory neurons, SV2A for synaptic signaling in inhibitory neurons, and MOG for myelination in oligodendrocytes in the cortex. These mechanisms also associate with learning and memory through pathway-based polygenic risk score modeling in ABCD. Our findings provide brain region- and cell type-specific insights into the complex regulatory network landscape of mTBI pathology and potential therapeutic candidates at the pathway and network levels.

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ObjectivePrevious research has yielded mixed findings regarding the validity of the Child Behavior Checklist (CBCL) DSM-Oriented Scales (DOSs) in identifying DSM diagnoses. The present study evaluates the concurrent validity of the DOSs by comparing scale classifications with a gold-standard clinical interview.MethodsParticipants ( = 11,851) were children in the NIH Adolescent Brain Cognitive Development (ABCD) study whose caregivers completed the CBCL and the Kiddie Schedule for Affective Disorders and Schizophrenia (KSADS) semi-structured interview at baseline (9.92 years, SD = 0.63), two-year follow-up (12.03 years, SD = 0.67), or both.Results2,321 (19.59%) children at baseline and 1,708 (15.57%) participants at two-year follow-up met criteria for one or more KSADS disorders. Sensitivity of the CBCL relative to KSADS diagnoses was generally low (10.36% – 75.00%), with only two scales above 50%. Specificity was high (92.47% – 97.07%). Positive predictive values were low (0.71% – 48.20%), and negative predictive values were high (89.84% – 99.90%). Area under the curve (AUC) ranged from 0.55 to 0.84.DiscussionIn the present sample, the DOSs showed poor concurrent validity with a gold standard clinical interview. Caution should be exercised when using the CBCL due to the high rates of false negatives.

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Early neurodevelopmental manifestations of genetic vulnerabilities to psychopathology are crucial for understanding disease onset and informing early intervention. However, the timing of when genetic risks begin to manifest in the brain remains unclear.

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Potentially traumatic events (PTEs) and substance use (SU) are commonly endorsed in early adolescence, a crucial period for neurodevelopment. PTEs and SU are precipitating events in the etiological development of comorbid posttraumatic stress disorder (PTSD) and substance use disorder (SUD). Separately, they have been shown to alter within- and between-network connectivity in the three brain networks posited by Menon’s Theory of Psychopathology: the default mode network (DMN), fronto-parietal network (FPN), and salience network (SN). While comorbid PTSD+SUD in adulthood shows shared neural underpinnings, this is less clear in adolescence. We analyzed the effects of PTEs and SU on resting state functional connectivity (rsFC) in 9-15 year olds from the Adolescent Brain Cognitive Development (ABCD) Study. Fixed effects panel models were fit to assess the effects of PTEs and SU on between-network (FPN-SN rsFC, DMN-SN rsFC, and FPN-DMN rsFC) and within-network (FPN rsFC, SN rsFC, and DMN rsFC) connectivity measured across three timepoints spanning two years. PTEs, SU, and their interaction was not significantly associated with between- and within-network rsFC two years later. No sex specific interactions were observed. Results suggest rsFC changes observed in older adolescents and adults with comorbid PTSD+SUD do not developmentally translate to early adolescents endorsing PTEs+SU. Lack of impact on rsFC may indicate a potential buffer period in which PTEs and SU do not affect rsFC until later in development or after symptom onset following PTEs+SU.

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Many adolescents initiate social media use during early adolescence, but the associations of early social media use with neurodevelopment have not been extensively studied. We utilized neuroimaging data from the U.S. Adolescent Brain and Cognitive Development (ABCD) Study to investigate the association of social media usage (hours per day) or social media addiction (Social Media Addiction Questionnaire) with brain morphology in early adolescence. We analyzed data from 7,614 participants with high-quality structural MRI and complete covariate data at Year 2 (2018-2020, ages 10-13). In addition to pre-defined cortical regions, we performed vertexwise analysis using Fast and Efficient Mixed Effects Algorithm (FEMA), which is unbiased by arbitrary borders between atlas-based brain regions and provides higher spatial resolution. After adjusting for demographics, socioeconomic factors, genetic ancestry, and scanner features, higher average daily social media use was significantly associated with lower total cortical thickness and volume. Region-of-interest (ROI) and vertexwise analysis identified broad regions with lower cortical thickness across the prefrontal cortices, temporal lobe, occipital lobe, and parietal lobe associated with both social media use and social media addiction, which overlap with key nodes of the default mode network, prefrontal executive control networks, and visual processing and attention networks. Social media addiction was not significantly associated with differences in brain morphology in ROI analysis. Our findings in a large nationwide population demonstrate that higher social media usage is associated with variation in cortical morphology, but future studies are required to establish the directionality of this association.

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Adolescent pain complaints may be related to genetic risk for chronic pain across the life course. Identifying whether adolescent pain is genetically linked to chronic pain in adulthood can advance understanding of pain etiology and inform early intervention. Two waves of pain assessments were used from the Adolescent Brain Cognitive Development (ABCD) study, a population-based sample of 11,876 adolescents with 94.0% retention across waves. The analyses included 6,387 adolescents of European-like ancestry (mean ages = 12.03 and 12.93 at waves 2 and 3; 52% males). Two polygenic scores (PGSs) were constructed using genome-wide association study summary statistics from up to 435,917 adults in the UK Biobank. One PGS captured shared genetic risk across 24 pain conditions (General Chronic Pain), while the second captured additional musculoskeletal-specific genetic risk across 11 conditions after adjusting for general pain (Musculoskeletal-specific Pain). Mixed-effects models were used to examine associations between these PGSs and adolescent self-reported pain presence, intensity, recurrence, and multi-site pain. Across both waves, 36.0%-37.0% adolescents reported pain. The General Pain PGS was associated with pain presence (b=0.07, OR=1.07, 95%CI=1.02-1.13, FDR-corrected p=0.023) and intensity (b=0.14, 95%CI=0.07-0.21, FDR-corrected p<0.001); but not recurrent pain (b=0.08, OR=1.08, 95%CI=1.01-1.16, FDR-corrected p=0.091) or multi-site pain (b=0.01, OR=1.00, 95%CI=0.94-1.07, FDR-corrected p=0.958). The Musculoskeletal-specific Pain PGS was not significantly associated with the outcomes. Genetic risk for chronic pain in adulthood, as measured by PGSs, is associated with adolescent pain complaints. Adolescent pain signals early vulnerability for chronic pain, highlighting adolescence for early intervention. PERSPECTIVE: This study links adolescent pain to polygenic risk for adult chronic pain, suggesting that early pain reflects enduring genetic liability and reflects central pain processes. These results provide mechanistic insight into chronic pain across the lifespan and highlight adolescence as a period for intervention.

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Significant changes occur in brain structure and cognition during adolescence. Investigating their association can provide insight into brain-based cognitive development, yet previous studies are limited by narrow measures, small samples, and lacking focus on age-dependence. Using a large cohort (n = 8534, age 9-15) with structural MRI and diffusion imaging, we derive 16 regional metrics and integrate them via morphometric similarity networks to characterize 16,563 brain features. We apply large-scale models to investigate their associations with seven cognitive subtests and general intelligence (g), as well as age-dependence. Brain areas most strongly associated with cognition also show the greatest age-dependence of the associations, primarily in the frontal, temporal, and occipital lobes. Stronger and more age-dependent associations with cognition are observed for structural MRI measures and global hub measures, compared with diffusion-derived metrics and local measures, respectively. Overall, our study provides a comprehensive and reliable characterization of adolescent brain structure-cognition associations.

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Accurate brain parcellation from structural MRI across the human lifespan is essential for advancing neuroimaging and neuroscience studies. However, existing methods often struggle to generalize owing to intensity and contrast variations across brain maturation, aging and differences in MRI acquisition protocols, limiting their clinical and research utility. Here we present BrainParc, a unified parcellation framework that leverages anatomical information invariant to intensity and contrast, enabling accurate, robust and longitudinally consistent parcellation across a heterogeneous dataset without the need for fine-tuning. Extensive experiments on both internal and external datasets demonstrate that BrainParc substantially outperforms state-of-the-art methods in delineating 106 brain regions. BrainParc consistently shows better performance across diverse populations and imaging conditions, both quantitatively and qualitatively. Beyond anatomical segmentation, we show that BrainParc enables reliable tracking of brain development and facilitates early diagnosis of neurological disorders, underscoring its potential as a robust and generalizable tool for large-scale neuroimaging studies and clinical translation.

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Attention-deficit hyperactivity disorder (ADHD) is a prevalent neurodevelopmental disorder characterised by inattention, hyperactivity and impulsivity, resulting in impaired functioning in multiple settings, including home, school and in social settings. Disparities exist in ADHD care among children, with White male children experiencing increased access to diagnosis and treatment. Other children remain underdiagnosed, undertreated and subject to poorer functional outcomes. Factors that impact equitable ADHD treatment include gender, race, ethnicity and social determinants of health (SDOH), including household income, parental education, insurance status, neighbourhood deprivation and discrimination. Medication is effective, yet little is known regarding the impact of medication type and trajectories of use on functional outcomes.

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Insufficient sleep (less than 8 hours for adolescents) has heterogeneous neurobiological underpinnings. Using the SuStaIn model on brain MRI from ABCD Study, we identified three distinct subtypes with reduced cortical thickness, starting from the postcentral, pericalcarine, and entorhinal cortices. The subtypes diverged in sleep-related determinants. The postcentral subtype mirrored the controls of sufficient sleep in sleep behavior and sleep environment and showed no psychiatric comorbidities, which aligned with natural short sleepers (phenotypically normal despite short sleep). Notably, this subtype displayed significantly advanced brain age, and polygenetic score analysis revealed a genetic predisposition for short sleep. The pericalcarine subtype was linked to environmental factors (e.g., light/noise pollution), with sleep duration mediating environmental effects on cortical thinning. The entorhinal subtype showed elevated psychiatric risk, younger brain age, and larger spatial correlations with psychosis-related neurotransmitter systems. This work deciphers the heterogeneous neurobiology of insufficient sleep and offers a framework for stratified interventions.

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Objective: Children with ADHD are at increased risk for developing gaming addiction, but the psychosocial mechanisms underlying this relationship remain poorly understood. This study aimed to identify factors that mediate this risk.

Method: We analyzed data from three consecutive waves (Years 2–4) of the Adolescent Brain Cognitive DevelopmentSM (ABCD®) Study, including approximately 7,260 participants. Linear mixed-effects models were used to assess the longitudinal association between ADHD diagnosis (measured via the Kiddie Schedule for Affective Disorders and Schizophrenia [KSADS]) and scores on the Video Game Addiction Questionnaire (VGAQ). A parallel mediation model was then employed to evaluate the role of nine psychosocial factors in mediating this relationship.

Results: Children with ADHD had significantly higher VGAQ scores over time, with an average increase of 1.3 points (p < 0.001) compared to those without ADHD. The mediation model identified three significant psychosocial mediators: prosocial peer involvement (7.4% of the total effect), school involvement (5.8%), and family conflict (5.1%).

Conclusion: Prosocial peer involvement, school engagement, and family conflict emerged as key psychosocial pathways linking ADHD to gaming addiction. These findings have important public health implications and suggest that strengthening peer networks and family environments may be effective targets for intervention in children with ADHD.

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Adolescent e-cigarette use remains an important public health challenge, and evidence on its neurocognitive effects at an early age is limited. This study examined associations between exclusive e-cigarette use and cognitive performance in adolescents.

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Emotion dysregulation (ED) is the inability to modulate the intensity and quality of emotional responses. It is strongly associated with psychopathology among youth, carries significant morbidity and predicts long-term impairments. Data on ED are limited among nonclinical populations. This study aims to estimate the prevalence of ED and to identify its demographic and clinical correlates in children.

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Delay discounting, or the propensity to devalue rewards as the time to reward receipt increases, is a robust predictor of psychiatric and neurodevelopmental outcomes across the life course. However, less is known about environmental antecedents that may be associated with delay discounting tendencies during adolescence, a developmental period during which delay discounting behaviors are still developing. Here, we examined the relation between delay discounting and the exposome—multi-level environmental exposures experienced from conception onwards. Participants included 9,848 children (Mage = 10.94 years, SD = 0.64; 53.2% female; 72% White) from the Adolescent Brain Cognitive Development Study who completed the Adjusting Delay Discounting Task at the 1-year follow-up. Predictors included six exposome factors that captured aspects of proximal and distal environments including: positive day-to-day experiences, family values, household adversity, neighborhood poverty, birth/pregnancy complications, and state-level conservatism/rurality. Greater household adversity, lower positive day-to-day experiences, and greater birth/pregnancy complications were associated with greater delay discounting, after adjusting for age, sex, race, household income and parent education. These findings highlight potential intervention and policy targets aimed at modifying delay discounting preferences in adolescence and reducing risk for negative sequelae across development.

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Sleep disturbances are increasingly recognized as a modifiable factor associated with poor outcomes after mild traumatic brain injury (mTBI) in adults, yet their prevalence, mechanisms, and clinical impact in children remain largely unknown. Identifying whether sleep problems contribute to behavioral, cognitive, and neurobiological outcomes after pediatric mTBI could inform targeted interventions.

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Background
In May 2021, COVID-19 vaccines became available for adolescents aged 12–15. However, safety concerns, misinformation, and politicization surrounding the vaccine left some parents hesitant to vaccinate their children. This study analyzes how media sources and religious affiliation were associated with parental COVID-19 vaccination intent.

Methods
We conducted a cross-sectional analysis of 5552 parents in the May 2021 COVID-19 Rapid Research Response Survey of the Adolescent Brain Cognitive Development (ABCD) study, which collected data on parental intention to vaccinate their children against COVID-19 just before the FDA approved the first vaccine for children aged 12–15. Parental vaccination intent was analyzed by media sources, religious affiliation, and other sociodemographic factors. We also fit a log-binomial regression model to examine the impact of media sources and religious affiliation on parental vaccination intent, controlling for sociodemographic factors.

Results
We found that, compared to parents consuming balanced media sources, parents consuming right-leaning media sources were less likely to plan to vaccinate their children [PR = 0.53 (0.47, 0.6)], while parents consuming left-leaning media sources were not significantly different from parents consuming balanced media [PR = 1.06 (0.99, 1.12)]. We also found differences in vaccination intent by religious affiliation. Compared to Christian parents, Agnostic/Atheist parents were more likely to plan to vaccinate their children [PR = 1.41 (1.35, 1.47)], as were Jewish parents [PR = 1.32 (1.22, 1.43)], and parents with no religious affiliation [(PR = 1.18 (1.14, 1.23)].

Conclusions
Our study highlights the multifaceted factors influencing vaccine hesitancy among parents of adolescents during the COVID-19 pandemic. To create effective public health strategies for future outbreaks, it is crucial to better understand the complex interplay of religious affiliation and media bias with vaccine hesitancy.

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Prenatal alcohol exposure (PAE) is a risk factor for early-onset psychopathology. Low birthweight (LBW), one potential consequence of PAE, increases the vulnerability of children for externalizing disorders. This study investigates potential sex-specific indirect pathways linking PAE to behavioral symptoms in offspring, focusing on LBW as a mediating and moderating factor.

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Introduction: Adolescent alcohol experimentation is a rising concern given its links to future problematic drug use. Difficulty with inhibitory control (i.e., the ability to suppress unwanted behaviors) is a well-known risk factor for early alcohol use onset. Nevertheless, little is known about the neurobiology of inhibitory control during early development (i.e., preadolescence), especially in relation to minimal early low-level alcohol use. The current study will reveal neural and behavioral differences in inhibitory control that differentiate youth will go on to engage in low-level alcohol experimentation compared with youth who remain alcohol naïve.

Methods: The current study examined 80 pairs of demographically and developmentally matched youth from the Adolescent Brain Cognitive Development Study to predict early alcohol experimentation, consuming at least one full drink, but no regular use, prospectively (ages 10–14 years old). To identify the underlying neural mechanisms differentiating youth who endorsed alcohol experimentation (AE) and those who did not (AN), we utilized impulsive personality trait markers and neurobehavioral markers from the Stop Signal Task.

Results: AE and AN youth showed no difference in task performance nor in impulsive personality traits but differed in patterns of neural engagement during the Stop Signal task. When compared to AN youth, AE youth displayed significantly higher activation in the right paracentral lobule and the left isthmus gyrus during the correct stop versus correct go contrast (indexing inhibitory control). Moreover, our findings indicated that, unlike in AN, a greater lack of planning in AE youth was associated with lower inhibitory control-related activation in the fusiform gyrus.

Discussion: This study demonstrates a possible role of neural correlates of inhibitory control that are associated with substance use initiation. Despite behavioral similarities, the study detects differential neural markers of inhibitory control between AE and AN youth, an effect potentially driven by impulsive personality trait markers. As these markers could be both constitutionally and environmentally based, our results suggest that early substance use is accompanied by detectable differences in brain activation in key regions, which may be similar to those in later stages of use, highlighting the importance of delaying the age of alcohol onset.

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Autism Spectrum Disorder (ASD) is a complex neurodevelopmental condition characterized by diverse presentations, which complicates the identification of consistent biological markers. This study examined whether integrating multimodal neuroimaging and physical-health measures from a population-based cohort can improve ASD classification and reveal interpretable markers that reflect both clinical and community variation.

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Numerous publications utilize data from the Adolescent Brain and Cognitive Development (ABCD) Study. This review aimed to evaluate how data from the ABCD cohort contributes to understanding the pathophysiology of incipient eating disorders.

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Family factors, such as parental symptomatology and parenting behaviors, are related to adolescent internalizing symptoms. Yet fewer studies have evaluated how family factors relate to the emergence of internalizing symptoms during the pubertal transition with large-scale longitudinal data. The present study addressed this issue using data from the Adolescent Brain Cognitive Development Study in adolescents who were prepubertal at baseline and had manifested puberty at 4-year follow-up (N = 2,276). Participants completed the Child Behavior Checklist (CBCL), Adult Self Report (ASR), Child Report of Parenting Behavior Inventory (CRPBI), Parental Monitoring Survey (PMQ), and Family Environment Scale (FES). Structural equation modeling revealed that higher levels of parent internalizing symptoms and parent-reported family conflict at baseline were associated with higher levels of adolescent internalizing symptoms at the 4-year follow-up. Higher baseline parental monitoring was associated with lower adolescent internalizing symptoms at the 4-year follow-up. Baseline parental acceptance and youth-reported family conflict were not related to adolescent internalizing symptoms. Adolescent sex did not moderate any associations in our models. Our results offer insights into how research, prevention, and intervention strategies can be developed to address the development of adolescent internalizing psychopathology.

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Problematic use of social media (PUSM) is a major public health concern estimated to affect 35% of adolescents. However, data-driven research to identify neural networks predictive of PUSM in adolescents remains limited. The aim of this study was to utilize connectome-based predictive modelling (CPM), a machine-learning approach that employs whole-brain functional connectivity data, to predict PUSM severity and identify underlying neural networks in adolescents. We included 2294 participants from the Adolescent Brain Cognitive Development study (M = 10.03, 50.6% female) who had resting-state functional magnetic resonance imaging (fMRI) data at baseline and PUSM scores at the four-year follow-up. CPM with 10-fold cross-validation was applied to resting-state fMRI data and PUSM scores. CPM successfully predicted PUSM scores and identified connectivity within and between multiple large-scale neural networks predictive of PUSM severity, which could be categorized into two key systems: (i) a cognitive control and self-regulation system consisting of the default mode, frontoparietal, and medial frontal networks, and (ii) a perceptual-motor integration system consisting of the visual area 1 and sensorimotor networks. The large-scale networks identified in the present study provide mechanistic insight into PUSM vulnerability and represent potential targets for personalized interventions. Future research should aim to replicate and extend the current results to refine prevention and treatment approaches.

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Many psychiatric disorders begin during adolescence, coinciding with the rapid development of brain white matter (WM). However, it remains unclear whether deviations from normal WM development during this period contribute to psychopathology. In this study, we developed normative models of brain age based on specific WM tracts using three large-scale developmental datasets ( ~ 10,000 subjects). We found that tract-specific deviations in WM development of association and limbic/subcortical systems were linked to concurrent and future cognition and psychopathology. The spatial pattern of the association system aligned closely with high-order brain networks and mitochondrial maps. Importantly, delayed brain-age especially in dorsal association tracts predicted psychiatric disorders across diagnoses and disorder onset over a 2-year follow-up. By identifying tract-specific WM development during preadolescence as a predictor of cognitive capacity and psychiatric risks, this study provides a framework for tracking individualized brain development and understanding the neurobiological underpinnings of cognition and transdiagnostic psychopathology.

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Objective
Despite increasing social media use among adolescents, few studies have investigated social media use patterns associated with the social media addiction (SMA) scale. SMA is characterized in terms of social media platforms, engagement patterns, and account settings.

Method
Cross-sectional data on youth ages 10-13 years from the Adolescent Brain Cognitive DevelopmentSM Study (n = 5,639) were used. The majority of the sample was female, White, and from families living above poverty. SMA was assessed via an adapted scale. Regression models assessed links between SMA and hours spent per day on social media, most-used platform, public and secret accounts, and follower and following counts.

Results
SMA was higher among youth whose most-used platforms were TikTok (b = 1.52, 95% CI 1.12, 1.93), Instagram (b = 0.92, 95% CI 0.51, 1.34), and Snapchat (b = 0.60, 95% CI 0.16, 1.03). Those with a public account (b = 0.85, 95% CI 0.56, 1.13), a secret account (b = 2.27, 95% CI 1.65, 2.89), or reporting more social media hours (b = 0.66, 95% CI 0.61, 0.71) had higher SMA scores. Weak interactions between social media hours and platforms were observed.

Conclusion
Higher SMA scores were most associated with TikTok, Instagram, and Snapchat use as well as using a public account, a secret account, and spending more time on social media. The relationship between social media hours and SMA confirms previous findings. This is the first study to investigate the relationship between account settings and SMA.

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Cyberbullying victimization is prevalent and closely linked to mental health problems. However, existing research, often limited by cross-sectional designs and a focus on direct relationships, has yielded inconsistent results. Furthermore, the biological mechanisms underlying the relationship between cyberbullying victimization and psychopathological outcomes remain largely unclear at present.

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Irritability, a form of emotion dysregulation, is a transdiagnostic symptom cutting across internalizing and externalizing problems. Clinical practitioners and parents have expressed concerns about the potential negative impact of screen use on irritability in youth. Despite the significant concerns, no studies have examined the association between screen usage and irritability and its directionality. Using a novel temporal network approach, this study investigated bidirectional associations between irritability and screen time across different activities in preadolescents.

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To investigate sex differences in prospective associations between eating disorder (ED) symptoms and changes in body mass index (BMI) percentile in early adolescence.

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Adolescence is a sensitive period of brain development marked by rapid cortical thinning and increased risk for psychiatric disorders, yet the biological drivers of atypical trajectories remain unclear. Here, using longitudinal data from the Adolescent Brain Cognitive Development Study, we examined whether genetic predisposition to systemic inflammation, indexed by polygenic scores for C-reactive protein (PGS-CRP), influences brain development and psychopathology. Higher PGS-CRP was associated with accelerated cortical thinning, particularly in medial temporal and insular regions, and with increased externalizing symptoms. Early-life infections independently predicted greater depressive and externalizing symptoms but did not interact with genetic risk. Mediation analyses indicated that cortical thinning partially accounted for the association between PGS-CRP and externalizing psychopathology. Biological annotation further identified the regional similarity between cortical effects of PGS-CRP and several neurotransmitter systems. Together, these findings suggest that genetic susceptibility to inflammation may shape adolescent brain maturation and contribute to mental health vulnerability via neuroimmune pathways.

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This study examines the association between parental mental health and children’s socioeconomic status (SES) across both home and school environments, using nationally representative data from the Adolescent Brain Cognitive Development (ABCD) Study. Traditional childhood SES markers often focus on parental income, occupational prestige, and maternal education; however, they may not fully capture how children’s proximal experiences of SES differ across daily contexts due to parents’ personal challenges. Employing latent variable path analyses (LVPA), we explored whether parents’ mental health, often a critical aspect of childhood adversity, shapes both home-based and school-based SES. Our findings revealed that poorer parental mental health is significantly linked to more disadvantaged SES in home and school settings. This suggests that parental mental health may affect not only the resources families possess but also the degree to which children benefit from those resources across critical developmental settings. These findings highlight the importance of addressing parental mental health as a key mechanism in understanding and reducing invisible developmental inequality.

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There is an urgent need to advance understanding of the neural underpinnings of depression, especially early in the life span. Examination of neural dynamics using resting-state functional magnetic resonance imaging (fMRI) data can provide indices of neural flexibility, which may provide important new insights for the neurobiology of pediatric depression. Here we applied Hidden Markov Modeling (HMM) to resting-state fMRI data to investigate neural flexibility in relation to depression and suicidal thinking in children. We utilized data from the Adolescent Brain Cognitive Development℠ Study (ABCD Study), and included data from 10,763 children (9-10 years) who completed two 5-min resting state fMRI scans at the baseline visit. After applying the NeuroMark framework to the data, HMM was applied with a varying number of states; a six-state model was selected from candidate models based on between-scan reliability. We applied linear mixed-effect modeling to test the relationship between two clinical predictors: current major depressive disorder (MDD) diagnosis and presence of suicidal ideation (SI) with our primary outcome for neural flexibility: the frequency of transitions between HMM-derived states (“state-switching”), while including sex, age, and other socio-demographic variables as covariates. Analyses were conducted both with and without correction for head motion. We also explored relationships with total time and dwell time in each state of the six states. Lower state-switching during rest was associated with both MDD and SI, although these findings were no longer significant after correcting for head motion. Notably, state-switching was inversely related to head motion and was higher in females than males. Exploratory analysis showed that MDD was associated with shorter dwell time in one state and longer dwell time in another, suggesting altered temporal persistence of specific neural configurations. Tentative evidence supported our hypothesis that lower state-switching in children with MDD and SI may reflect a reduction in brain flexibility, potentially contributing to a tendency to become “stuck” in negative patterns of thinking and feeling. However, the relatively low frequency of these problems in late childhood reduced statistical power after correcting for motion. Future research is needed to assess these relationships at later adolescent time points, when higher prevalence of depression and SI and lower prevalence of head motion will allow more powerful tests of these associations.

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Emerging evidence suggests regional neuroanatomical variability may be predictive of early alcohol use (before age 15). However, the relationship between whole-brain network organization and early alcohol initiation remains unknown. Using data from the Adolescent Brain Cognitive Development (ABCD) study, we conducted a structural covariance network (SCN) analysis to examine brain network features preceding early alcohol initiation. Structural MRI data collected at baseline (ages 9-10) were used to generate SCNs based on regional cortical thickness measurements. Early alcohol initiation was defined as consuming a full drink between baseline and 4-year follow-up ( ≤ age 15). Participants who reported a full drink of alcohol at baseline, did not participate in the 4-year follow-up, or did not meet imaging quality control criteria were excluded. The remaining participants were compared to a subsample matched at a 1:1 ratio (n = 160 per group). SCN properties, including network segregation (modularity, clustering coefficient), integration (characteristic path length, global efficiency), and resilience (degree assortativity), were compared between groups. While no differences in regional cortical thickness between groups were identified, early initiators demonstrated lower segregation and higher integration compared to non-initiators. These findings suggest that cortical thickness network topology at ages 9-10 may serve as a neuroanatomical risk marker for early adolescent alcohol initiation, independent of prior alcohol exposure, sociodemographic differences, and regional neuroanatomical variability.

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Deviant peer association is a robust risk factor for offending, that is, any behavior that violates a criminal law. This can include behaviors like drug use, violence, and theft; among others. Autism is a neurodivergent condition characterized by both atypical cognitive development and challenges with social interaction and communication. Despite these impairments, there is a dearth of research focused on the relationship between autism and deviant peer association. Relatedly, there exists no research examining the role that dual systems model constructs (sensation-seeking and impulse control) as mediators of this relationship. This study sought to address these gaps in the literature by examining autism as a predictor of deviant peer association in childhood and whether either or both impulse control or sensation-seeking significantly mediate this relationship.

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Characterizing associations between individual differences in brain activity and behavior remains a primary challenge in functional neuroimaging research. A growing literature supports the use of formal computational models to represent the mechanistic processes underlying behavior during cognitive tasks. This study applies one such model to the Adolescent Brain Cognitive Development Study stop-signal task (SST) and quantifies relationships between mechanistic model parameters and task-related brain activation using a machine-learning-based predictive modeling approach. With a large sample of task performance and task-related neuroimaging data from 9- to 11-year-olds (n = 6469), we found that SST formal model parameters showed relatively strong relationships with fMRI task-related activation (average variance explained as high as R2 = 26.86 ± 1.69%) compared with empirically derived performance measures (largest R2 = 20.89 ± 1.41%). Our approach suggests that neuroimaging data are most closely associated with evidence accumulation for the go choice process and with attentional lapses that prevent the initiation of the stop process (“trigger failure”). Increased salience network (i.e., insula and anterior cingulate) activity on correct go trials was associated with worse evidence accumulation, and greater visual cortex activity on error trials was associated with fewer attentional lapses. In addition, through relationships with phenotypic measures of inhibition, impulsivity, and cognition, we provide evidence supporting the formal model’s construct validity. We demonstrate the utility of computational cognitive modeling for revealing stronger, and more meaningful, associations between brain function and behavior.

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Preclinical evidence suggests that intrauterine exposures can impact hypothalamic structure at birth and future disease risk, yet early human data are limited. Because the hypothalamus regulates critical early life processes including sleep, growth, stress regulation, and metabolic control, characterizing its structural maturation and how it relates to developmental conditions and exposures is essential for understanding links to later health.

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There are limited large-scale, prospective analyses examining problematic (addiction-like) screen use and mental and behavioral health outcomes in early adolescents. This study aimed to determine the associations between problematic screen use and mental and behavioral health outcomes-such as depressive symptoms, suicidal behaviors, sleep disturbance, and substance use initiation-1 year later in a national cohort of children aged 11-12 years in the U.S.

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Objective
Impulsivity, a key symptom in attention-deficit/hyperactivity disorder (ADHD), is related to maladaptive outcomes longitudinally. Yet relatively little is known about how impulsivity manifests among children with the ADHD primarily inattentive presentation. We sought to address this gap by investigating impulsivity symptoms across all ADHD subtypes and in youth without ADHD. We also examined the association between ADHD symptoms at baseline and maladaptive outcomes measured cumulatively over 4 years.

Method
We examined impulsivity symptoms and maladaptive outcomes measured longitudinally among 5059 youth with complete diagnostic and symptom data, age 9-10 from the Adolescent Brain Cognitive Development℠ (ABCD) Study.

Results
Youth with the ADHD inattentive presentation demonstrated elevated impulsivity relative to typically developing youth across self (Cohen’s d=0.489, 95% confidence interval (CI) [0.40, 0.58], p<0.00001) and parent reports (d=1.40, 95% CI [1.31, 1.50], 95% p<0.00001) as well as decreased performance relative to typically developing youth on measures of impulsivity control (flanker: d=-0.251, 95% CI [-0.35, -0.16], p<0.0001; stop signal task: d=-0.276, 95% CI [-0.38, -0.17], p<0.00001). Among youth with the inattentive presentation, impulsivity measured at study baseline was associated with increased risk for maladaptive outcomes after controlling for hyperactivity and inattentive symptoms.

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Impulsivity symptoms among youth with the inattentive ADHD presentation are higher than traditionally conceived. Longitudinal associations between impulsivity and maladaptive outcomes underscores the clinical import of elevated impulsivity symptoms in youth with the inattentive presentations. We highlight the importance of classifying impulsivity symptoms independently of hyperactivity symptoms to facilitate accurate identification of individualized symptom profiles for the purpose of personalized treatment planning and risk evaluation, and to advance future research.

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Physical activity and sedentary behavior are associated with adolescent mental health. However, prior studies have not assessed whether these associations differ across varying levels of mental health severity. This study uses objectively measured physical activity and sedentary behavior to examine their associations with adolescent mental health and to determine how these associations vary across the distribution of mental health symptoms.

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Low socioeconomic status (SES) is linked to pubertal development, mental health issues, and academic performance. However, the role of early pubertal development in the link between low SES and mental health and academic outcomes is unclear. Using longitudinal data from the ABCD Study (9-10 years at baseline, = 9,848, 52.2% males) across four time points, we examined associations between household and neighborhood disadvantage, pubertal development, and mental health and academic achievement. Greater household and neighborhood disadvantage were associated with more advanced pubertal status at baseline in both males and females. Among females, higher pubertal status at baseline mediated the association between lower household income and neighborhood disadvantage with greater mental health problems and poorer school performance. Additionally, slower pubertal tempo attenuated the relationship between neighborhood disadvantage and these outcomes in females. These findings underscore the importance of considering both household and neighborhood contexts in shaping adolescent development and highlight pubertal development as a potential pathway underlying socioeconomic disparities in mental health and academic achievement.

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Adolescent depression has risen sharply, especially among racial-ethnic minority youth. While racial-ethnic discrimination is known to be linked with depression, there is limited understanding of how individual differences in brain development contribute to this process. Drawing on the framework of adolescent neurobiological susceptibility, this study examined the moderating role of hippocampal volume in the longitudinal association between racial-ethnic discrimination and adolescent depression. Using longitudinal data of racial-ethnic minority youth from the Adolescent Brain Cognitive Development study (n = 5,061, M = 9.93 years; 52% female), we found that racial-ethnic discrimination was associated with adolescents’ increased depression two years later. Notably, a larger left hippocampal volume amplified the link between discrimination and depression. These findings highlight the detrimental role of racial-ethnic discrimination on adolescents’ psychological well-being and suggest that hippocampal volume may serve as a neurobiological marker of susceptibility, amplifying the negative impact of racialethnic discrimination among racial-ethnic minority youth.

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The World Health Organization ranks depression as the leading non-fatal contributor to the global burden of disease. Research shows that early intervention before clinical onset leads to better outcomes. To study depression at this pre-onset stage, risk can be evaluated through depressive prodromal behaviors and associated brain biomarkers. Both environmental and genetic factors independently contribute to depression vulnerability, yet little work has examined how they interact. We therefore examined whether the socioeconomic status (SES) predictor of family income-to-needs ratio (INR) has independent and/or interactive effects with a depression polygenic risk score (D-PRS) on youth behavior and brain structure and function.

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Normative modeling has been applied to study how brain measures, such as gray matter thickness or volume, change across development. These models help identify how an individual’s brain may differ from what is typical for their age or sex, which could eventually support more personalized treatments. However, most existing models use only one-time (cross-sectional) data, meaning they cannot capture how the brain changes over time. Longitudinal data, tracking the same individuals across multiple time points, is more informative but harder and more expensive to collect. We analyzed brain scans from over 6000 young people in the Adolescent Brain Cognitive Development (ABCD) study, about half of whom were girls. Each participant had brain scans at the start of the study, two and four years later. We deployed Baseline-Conditioned Norms (B-Norms) that used cortical thickness derived from each person’s first scan and their ages at baseline and follow-up timepoint to predict cortical thickness at follow-up. We compared this to Cross-Sectional Norms (C-Norm), which only used age to predict thickness at follow-up. As expected, B-Norms predicted cortical thickness more accurately. Importantly, they were also better at detecting brain differences linked to puberty, especially in girls. Our findings suggest that our here proposed B-Norms may capture more developmental variance and may be more sensitive to sex-specific brain development over time during puberty. Therefore, B-norms may constitute a valuable complement to established C-norms.

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Social media exposure may influence early nicotine experimentation, a behavior linked to later nicotine dependence and health risks. Few studies have examined the role of smoking expectancies (i.e., beliefs about the anticipated positive or negative effects of nicotine) as a pathway underlying this association, especially in early adolescence. The objective of this study is to examine the prospective association between social media use and nicotine experimentation in early adolescence, and whether smoking expectancies mediate this relationship.

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The cultural value of familism describes prioritizing family over the individual. Previous evidence supports relations between familism and health behaviors, including sleep. Using data from the Adolescent Brain Cognitive Development Study, this investigation explored associations of parent and adolescent familism and adolescent sleep. The sample included 438 Latino/a parent-adolescent dyads, with youth averaging 11.87 ( = 0.67) years old (assigned female at birth: 49.78%) and parents averaging 40.51 ( = 6.50) years old (female: 90.38%) with a majority identifying as Mexican or Mexican American (parents: 53.83%; youth: 54.51%). Most adolescents were born in the United States or its territories (94.28%). Parents and adolescents independently reported on multiple dimensions of familism, including familism support, familism obligation, and familism referent, which were combined to create an overall familism score. Adolescents wore Fitbit devices that measured objective parameters of sleep including minutes, efficiency, wake after sleep onset, latency, midpoint, and variability in minutes and midpoint. Multiple regression models were fit to determine associations of parent and adolescent familism dimensions with adolescent sleep. Youth obligation and parent support familism were related to more ideal sleep, while youth referent and parent obligation familism were related to less ideal sleep. While some dimensions of familism may pose a risk for poor sleep, others support ideal sleep and should be emphasized within the parent-adolescent relationship. As practitioners and clinicians incorporate cultural sensitivity into their practices and recommendations and families cultivate a supportive environment through familism values, Latino/a youth will be more likely to experience optimal sleep outcomes. (PsycInfo Database Record (c) 2026 APA, all rights reserved).

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Attention deficit hyperactivity disorder (ADHD) is a prevalent neurodevelopmental disorder. Studies indicate that 20-55 % of individuals with ADHD experience comorbid sleep disturbances, among which, sleep initiation difficulty (SID) is highly correlated with hyperactivity behaviors. However, the underlying neuroimaging mechanisms common to ADHD and sleep initiation difficulty remain poorly understood.

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Depression is shaped by both genetic and environmental factors, but genome-wide interaction studies (GWIS) often lack power to detect complex gene-environment (G × E) interactions. We applied a forest-based machine learning approach to 38,018 UK Biobank (UKB) participants, examining interactions between 285,677 single-nucleotide polymorphisms (SNPs) and three trauma types (childhood, adult, and catastrophic trauma). While GWIS detected no significant interactions, we identified 8,225 potentially important SNP-environment pairs across 1,732 genes, with childhood trauma contributing most prominently. Stratified heritability was higher among childhood trauma-exposed individuals (13.3%) versus those unexposed (6.0%). Many identified genes overlapped with known psychiatric risk loci and accounted for most of the SNP-based heritability. Thirteen top genes were replicated in the Adolescent Brain Cognitive Development Study. Our findings highlight the polygenic G × E nature of depression and the critical role of childhood trauma in modulating genetic risk, demonstrating the value of forest-based methods in detecting complex gene-environment interactions.

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Neurodevelopmental models regard impulsivity as a central risk factor for adolescent substance use. However, the practical utility of impulsivity in predicting substance use is complicated by variability among measures that encompass multiple methods and theoretical domains. Prior research has been constrained by cross-sectional designs, small sample sizes, and/or the use of a narrow subset of impulsivity measures.

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This study relied on previously established factor scores of environmental, education, and socioeconomic-related variables in the Adolescent Brain Cognitive Development Study (ABCD) and their associations with cognitive functioning in youth.

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Social health, having an adequate quantity and quality of social relationships, is essential for well-being but understudied during adolescence compared to adulthood. We sought to identify patterns and predictors of social health by characterizing peer relationships among 10,050 adolescents (10-13 years old, 4,815 girls, 53.68% non-Hispanic White) in Year 2 of the Adolescent Brain Cognitive Development Study. To characterize social health profiles, we applied latent profile analysis on peer variables collected in Year 2: number of friends (close, general), aggression, victimization, relationships with prosocial and rule-breaking peers, and support. We then assessed whether loneliness (baseline, Year 2), family conflict (baseline, Year 2), and participant sex predicted profile membership. Fit indices supported a three-class solution: a “selective” class (∼60% of the sample) characterized by values below sample means but within population norms across variables (e.g., number of friends), a “robust” class (∼30%) characterized by high numbers of friends, and a “concerning” class (∼10%) characterized by high levels of peer aggression and victimization. Lonely adolescents were more likely to be in the concerning group and less likely to be in the robust group. Youth with more family conflict and boys were more likely to be in the concerning group; girls were more likely to be in the selective group. These findings reveal profiles of peer relationships in a large representative sample, providing a template for characterizing social health as adolescents begin to build intimate peer relationships. The results also highlight individual differences in social health profiles, which can inform targets to improve adolescent social health. (PsycInfo Database Record (c) 2026 APA, all rights reserved).

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Graph deep learning models, a class of AI-driven approaches employing a message aggregation mechanism, have gained popularity for analyzing the functional brain connectome in neuroimaging. However, their actual effectiveness remains unclear. In this study, we re-examine graph deep learning versus classical machine learning models based on four large-scale neuroimaging studies. Surprisingly, we find that the message aggregation mechanism, a hallmark of graph deep learning models, does not help with predictive performance as typically assumed, but rather consistently degrades it. To address this issue, we propose a hybrid model combining a linear model with a graph attention network through dual pathways, achieving robust predictions and enhanced interpretability by revealing both localized and global neural connectivity patterns. Our findings urge caution in adopting complex deep learning models for functional brain connectome analysis, emphasizing the need for rigorous experimental designs to establish tangible performance gains and perhaps more importantly, to pursue improvements in model interpretability.

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Household cannabis use is a risk factor for adolescents’ mental health problems. However, little is known about the association of the cessation and psychological impairments in affected adolescents. This study examined the associations of household cannabis cessation and adolescents’ mental health outcomes and potential pathways.

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The environment, especially social features, plays a key role in shaping the development of the brain, notably during adolescence. To better understand variation in brain-environment coupling and its associated outcomes, we identified ”social envirotypes,” or different patterns of social environment experience, in the Adolescent Brain Cognitive Development Study by hierarchically clustering subjects. Two focal clusters, which accounted for 89.3% of all participants, differed significantly on eight out of nine youth-report social environment quality measures, representing almost perfect complements. We then applied tools from network neuroscience to show different social envirotypes are associated with different patterns of whole brain functional connectivity. Differences were distributed across the brain but were especially prominent in Default and Somatomotor Hand systems for these focal clusters. Finally, we examined how social envirotypes change over development and how these patterns of change are associated with a suite of outcomes. The resulting dynamic social envirotypes differed along dimensions of stability and quality, but outcomes diverged based on stability. Altogether, our findings represent significant contributions to both social developmental neuroscience and network neuroscience, emphasizing the variability and dynamicity of brain-environment coupling and its consequences.

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Puberty is a critical developmental process that is associated with changes in pubertal (or steroid) hormone levels, which are believed to influence adolescent behaviour via their effects on the developing brain. So far, there are limited and inconsistent findings regarding the relationship between steroid hormones and brain structure and function in adolescent females, with many existing studies employing small sample sizes. Thus, in this study, we explored the association between oestradiol (E2), testosterone (Tes), and dehydroepiandrosterone (DHEA) and brain structure (gray matter volume, sulcal depth, cortical thickness, and white matter microstructure) and function (resting-state connectivity, emotional n-back task-related function) in 3024 adolescent females (age 8.92-13.33 years, mean age (SD) = 10.37 (0.94) years) from the Adolescent Brain Cognitive Development^SM (ABCD) Study. We used elastic-net regression with cross-validation to investigate associations between hormones and brain phenotypes derived from multiple imaging modalities. We found that structural brain features, including cortical thickness, sulcal depth, and white matter microstructure, and resting state connectivity between cortical networks and subcortical regions, were important features associated with hormones. E2 was most strongly associated with prefrontal and premotor regions involved in working memory and emotion processing, while Tes and DHEA were most strongly associated with parietal and occipital regions involved in visuospatial functioning. All three hormones were also associated with prefrontal, temporoparietal junction, and insula cortices. Thus, using an advanced methodological approach, this study suggests both unique and overlapping neural correlates of pubertal hormones in adolescent females and sheds light on the mechanisms by which puberty influences adolescent development and behaviour.

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Internalizing symptoms are common in childhood and linked to meaningful differences in brain structure, yet their organization and neurobiological correlates during this developmental period remain poorly understood. An increasing number of studies conceptualize internalizing psychopathology as dimensional, transdiagnostic, and hierarchical, yet the factor structure of these symptoms in youth remains to be clearly defined. Additionally, the neurostructural underpinnings of internalizing factors warrants further investigation in younger samples. Using a large sample (N = 11,868) of 9- to 10-year-old children from the Adolescent Brain Cognitive Development (ABCD Study), we examined the factor structure of internalizing symptoms and identified associated neurostructural correlates, focusing on regional gray matter volume, cortical thickness, and cortical surface area. Higher-order modeling was used, in which the correlations among first-order factors for distress, cognitive, fear, and somatic symptoms were accounted for by a higher-order general internalizing factor. After controlling for age, sex, income, parental education, and site/MRI scanner, we found that general internalizing, distress, and cognitive symptoms were associated with smaller gray matter volume and cortical surface area across most regions. Fear symptoms showed a more localized pattern of smaller surface area in the parietal, temporal, and insular cortices. Cortical thickness and somatic symptoms showed less consistent associations. These findings contribute to the growing literature on dimensional models of internalizing psychopathology in youth by linking higher- and lower-order internalizing symptom factors to distinct patterns of neurostructural variation. Our results support the utility of hierarchical dimensional approaches for elucidating the neural substrates of internalizing symptoms during middle childhood.

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Violence affects over one billion children globally each year. Early adolescence is a sensitive period for neurobehavioral development, making it critical to understand how violence impacts the brain. While emotional, physical, and social outcomes related to violence have been extensively studied, the neurobiological mechanisms linking violence to developmental outcomes remain underexplored. This study investigated associations between violence and neural communication in 9-10 year olds from the longitudinal Adolescent Brain Cognitive Development-Social Development Study (n = 2016). Regression analyses tested whether lifetime violence exposure (ages 9-10), recent exposure (ages 11-13), and cumulative exposures over three years were associated with connectivity between critical networks and subcortical regions. Findings revealed distinct types of violence were associated with alterations in brain connectivity across critical networks involved in emotional regulation, cognitive control, and threat detection. Internet victimization was consistently associated with alterations in neural communication, suggesting digital environments may uniquely influence neural pathways linked to self-reflection and emotional processing. Cumulative violence exposure was associated with greater increases in progression of neural communication between the default mode and salience networks and the salience network and hippocampus. These findings emphasize the need for tailored interventions addressing specific violence exposures, mitigating potential impacts on youth brain development and emotional health.

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Cannabis positive expectancies, favourable beliefs about cannabis effects, are a key risk factor for cannabis initiation and problematic use during adolescence. Prior research demonstrated a robust association between cannabis positive expectancies and increased use among adolescents, yet less is known about the developmental aetiology, biobehavioural mechanisms and cognitive context that contribute to these expectancies. The present study examines the intermediary role of negative urgency, a facet of impulsivity characterized by rash action under distress. Additionally, the study investigates whether anterior cingulate cortex (ACC) activation during emotional reward processing moderates this indirect effect. We conducted a longitudinal moderated mediation model with three waves of data from the Adolescent Brain and Cognitive Development (ABCD) study, analysing 6638 youths (baseline M = 10.1 years; 47.8% female). Family conflict at baseline predicted increased cannabis positive expectancies ΔT5T7 through increases in negative urgency at T5 (β = 0.017, p < 0.001, 95% CI [0.045, 0.069]). Heightened ACC activity at T5 (anticipatory large loss), including bilateral caudal and rostral regions, intensified negative urgency’s impact on cannabis positive expectancy ΔT5T7: Left caudal (β = 0.081, p < 0.001, 95% CI [0.041, 0.122]), right caudal (β = 0.062, p = 0.004, 95% CI [0.020, 0.105]), right rostral (β = 0.041, p = 0.026, 95% CI [0.001, 0.081]) and left rostral (β = 0.052, p = 0.01, 95% CI [0.012, 0.092]). This study highlights how neural activity amplifies stress-related effects on adolescent substance use expectations, suggesting emotional decision-making as a target for prevention.

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This study aims to investigate the roles of decision-making processes and genetics in the co-occurrence of alcohol use and suicidal thoughts/behaviors (STB) in adolescence. We used data from the ABCD study (abcdstudy.org) and included behavioral (computerized tasks, self-report questionnaires) and genetic (polygenic scores [PGS]) measures related to cognitive (executive functions) and affective (delay-discounting, risk-taking, impulsivity) processes involved in decision-making. First, we evaluated the latent structure of decision-making in the full sample (N = 11,868) using a split-half exploratory and confirmatory factor analysis. Second, we evaluated the association between alcohol experimentation ( > 1 sip) and STB in three genetically-defined ancestry groups: European (EUR, N = 6080), African (AFR, N = 2085), and the Americas (AMR, N = 2712). We used logistic regressions to examine which PGS and behavioral factors were related to STB and tested the mediational effect of behavioral processes. STB prevalence was between 0.85-4.17%. Decision-making was best represented by three latent factors: cognitive, emotional-impulsivity, and premeditation-perseverance. Regression analyses showed that alcohol experimentation was related to STB in EUR only (OR = 1.44, 95%CI = 1.10;1.89). Lower tendencies on the emotional-impulsivity factor were related to lower STB in all groups (ORs 0.69-0.77), and better premeditation-perseverance were associated with lower STB in EUR (OR = 0.57) and AFR (OR = 0.72). In EUR, the association between alcohol experimentation and STB was mediated by the emotional-impulsivity (15.33%) and premeditation-perseverance (22.60%) latent factors. The associations between PGS for externalizing behaviors and STB also acted through the emotional impulsivity and perseverance-premeditation factors (mediations 6.98-10.30%). These findings suggest that decision-making-related processes may contribute to the alcohol use-STB co-occurrence.

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Emerging evidence suggests that adolescents with depression may experience cognitive dysfunction. However, studies are primarily cross-sectional and few in number. This study examines the temporal association of depression and cognitive function among participants of the Adolescent Brain Cognitive Development Study.

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This review synthesizes ten years of research utilizing data from the Adolescent Brain Cognitive Development (ABCD) Study, emphasizing how the study’s comprehensive, longitudinal design supports a multivariate understanding of adolescent mental health. We focus on studies that have examined the collective or interacting relations of multiple factors to mental health in adolescents, as this unique dataset allows for examining more complex configurations of risk factors. We highlight key findings from ABCD data that have deepened our understanding of the risk factors shaping mental health outcomes in adolescence. Findings underscore the complex interplay of biological, psychological, and/or contextual factors on adolescent mental health. We conclude with a forward-looking discussion of emerging research priorities and opportunities to further leverage the ABCD dataset to inform developmental theory, prevention, and intervention efforts.

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Problematic gaming has been linked to increased levels of psychotic-like experiences (PLEs) in youth, but the role of environmental factors remains unclear. We aimed to examine the association of problematic gaming with PLEs and, using affordance theory, to evaluate whether environmental factors could help enhance the identification of this risk.

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This study examined cross-sectional and prospective differences in mental health and family functioning among caregivers aware of their child’s self-injurious thoughts and behaviors (SITBs), caregivers unaware of their child’s SITBs, and caregivers of children without SITBs. Data were drawn from an epidemiological U.S. sample of children (ages 9-10) and their caregivers who participated in three yearly assessments as part of the Adolescent Brain Cognitive Development study ( = 11,303, 47.6% female). Caregivers reported on their own mental health problems and SITBs, their child’s SITBs, and family conflict. Children reported on their own SITBs, family conflict, parental monitoring, and parental acceptance. Compared to caregivers of children without SITBs (81%), both aware (9.9%) and unaware (9.1%) caregivers reported more externalizing problems at baseline. Their children reported more family conflict and lower parental monitoring and acceptance across assessments. Relative to unaware caregivers and caregivers of children without SITBs, aware caregivers reported elevated internalizing problems at baseline and greater odds of engaging in SITBs at baseline and follow-up. Compared to children of unaware caregivers, children of aware caregivers reported lower family conflict and higher parental monitoring and acceptance at baseline. In contrast, aware caregivers reported higher family conflict at baseline and 1 year later compared to unaware caregivers. Overall, caregivers of children with SITBs, whether aware or unaware, experienced more mental health problems and long-term effects on family functioning. Aware caregivers also reported higher SITB risk. Family-based interventions with a focus on caregivers’ mental health may help reduce children’s SITBs and family suffering. (PsycInfo Database Record (c) 2026 APA, all rights reserved).

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Youth suicide is increasingly prevalent, is a leading cause of death, and its public health burden is acute. Juvenile Legal System (JLS) involvement is an established correlate of suicidality; however, it is unclear how JLS involvement is nomologically associated with suicidality. Adolescents are situated within ecological contexts (i.e., family, schools, neighborhoods) that likely interact to modify the association of JLS involvement and suicidality. To improve predictive models, rigorous prosecution of this relationship must disentangle related risk/protective factors (i.e., sex/gender, race-ethnicity, discrimination, trauma, familism). Based on 2426 adolescents enrolled in a substudy of the Adolescent Brain and Cognitive Development Study (ABCD), we utilized propensity score matching to test the association of police contact at 10-13 years-old with suicidal outcomes (i.e., self-harm, suicidal ideation, suicide attempt) two years later, covarying for age, education, race-ethnicity, sex/gender, discrimination, adverse childhood events (ACEs), and familism. After adjusting for numerous demographic, experiential, and family-level correlates, police contact did not significantly predict suicidal outcomes two years later. Baseline ACEs positively predicted self-harm and suicidal ideation two years later. Lower familism predicted self-harm, suicidal ideation, and suicide attempts two years later. With inclusion of important risk and protective factors, JLS involvement did not uniquely predict suicidality. Factors closely related to JLS involvement (i.e., ACEs, familism) incremented risk. To address the increasing prevalence of suicidality and the disproportionate impact of suicide on JLS-impacted youth, it is critical to investigate individual and systemic factors, and how they interact, to increase risk for suicidality.

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Despite the rapid growth in gaming consumption and associated harms in adolescents, data-driven research to identify brain networks underlying problematic gaming remains limited. This study aimed to identify neural networks predictive of problematic-gaming severity in youth using connectome-based predictive modelling (CPM), a machine-learning approach that employs whole-brain functional connectivity data.

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Much of prior literature examines potentially traumatic event (PTE) exposure as a cumulative risk, though PTEs may not have an equal impact on substance use (SU). In the current study, we test McLaughlin & Sheridan’s (2016) model in a sample of 11,800 community youth (ages 9-15 years old) enrolled in the nationwide, longitudinal Adolescent Brain Cognitive Development (ABCD) Study to examine the impact of PTE types on SU. We analyze concurrent associations between PTE types (physical abuse, domestic violence, community violence, emotional neglect, poverty, and institutionalization / deprivation) and substance use (pooling alcohol, cannabis, or nicotine) and prospective associations whereby exposure to different PTE types predicts SU one year later (self-medication hypothesis). For concurrent associations, we find emotional neglect and physical abuse were significantly positively related to SU. In terms of prospective associations, institutionalization / deprivation, emotional neglect, and physical abuse significantly positively predicted SU. A majority of associations between PTE types and SU were accounted for by other PTE types and time-varying covariates (e.g., internalizing/externalizing symptoms). The association between PTEs and SU during adolescence varies across PTE types. PTEs categorized as physical abuse and emotional neglect are more likely to lead to SU. Findings suggest that surveillance for SU is especially warranted in youth experiencing emotional neglect and physical abuse relative to other PTEs. Future research should examine more types of PTEs along a wider age span to replicate findings.

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BACKGROUND
Children spend significant amounts of time using digital media (DM), and longer exposure may increase attention-deficit/hyperactivity disorder (ADHD)-related symptoms, although findings are mixed. We investigated longitudinal association between different types of DM use and ADHD-related symptoms in school-aged children, accounting for genetic predisposition and socioeconomic status.

METHODS
This study included children from the Adolescent Brain Cognitive Development Study, and these children were followed annually for 4 years. Estimated time spent on social media, video games, and television/videos was self-reported using Youth Screen Time Survey. ADHD-related symptoms were assessed at each visit with the parent-reported Child Behavior Checklist. Genetic predisposition was estimated using a polygenic risk score for ADHD (PGS-ADHD).

RESULTS
The study included 8324 children (53% boys; mean age: 9.9 years). On average, children spent 2.3 hours/d watching television/videos, 1.4 hours/d on social media, and 1.5 hours/d playing video games. Average social media use was associated with increased inattention symptoms over time (β [SE], 0.03 [0.01]; P < .001), with a cumulative 4-year effect of β = 0.15 (SE, 0.03; P < .001). No associations were found between playing video games or watching television/videos and ADHD-related symptoms. The association between social media use and inattention symptoms was not moderated by sex, ADHD diagnosis, PGS-ADHD, or ADHD medication status. Inattention symptoms were not associated with increased social media use over time.

CONCLUSION
Social media use was associated with an increase in inattention symptoms in children over time. Although the observed effect size was small, it could have significant consequences if behavior changes occur at the population level.

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Experimentation with alcohol and other substances during the early adolescent period is associated with a myriad of potentially deleterious health outcomes. The present analysis utilized data from the Adolescent Brain and Cognitive Development Study (ABCD Study®) to investigate the relationships between risk perception, susceptibility to peer influence, and substance use in early adolescence.

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This study aimed to explore potential mediation pathways between racial/ethnic discrimination experience and cannabis use intention through perceived cannabis accessibility and then perceived harm. Preteens ( = 2,690, ages 9-13) from the Adolescent Brain Cognitive Development Study (Release 4.0) were included. Structural equation modeling was conducted. Experiencing racial/ethnic discrimination was associated with higher cannabis use intention ( = 0.068,  < 0.05). Preteens who experienced racial/ethnic discrimination were more likely to perceive cannabis as more accessible ( = 0.134,  < 0.05), resulting in lower perceived harm (=-0.123,  < 0.001), which subsequently increased cannabis use intention (=-0.085,  < 0.001). These results emphasize the need for interventions to address discrimination-related trauma in preteens.

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Early life adversities (ELAs) including experiences such as abuse, neglect, and household dysfunction are strongly linked to psychopathology; yet, the developmental pathways connecting ELA to externalizing and internalizing psychopathology remain unclear. While most research has focused on threat and negative affect, positive emotions may represent a critical but understudied mechanism linking ELA to mental health outcomes.

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Early life adversity (ELA) has been linked to shifts in developmental pace. This study examined whether brain maturity during early adolescence was influenced by ELA, and whether it explained the relationship between ELA and mental health problems. A sample (n = 7658, 46 % female) from the Adolescent Brain and Cognitive Development (ABCD) Study was utilized, with data collected at three time points spanning 9-14 years of age. Exposure to threat, psychosocial deprivation, household instability, and socioeconomic stress were measured at baseline. A predictive model of normative brain development (brain age) trained on a large independent lifespan sample was applied to structural neuroimaging data from the second timepoint. Brain-age-gap (BAG) – the difference between model predicted brain age and chronological age – was tested as a mediator of adversity exposure and internalizing/externalizing problems at the third timepoint. A more positive BAG was associated with more externalizing problems, but hypothesized associations between adversity and BAG were not significant. Sex moderation of these pathways suggests adversity may differentially affect the pace of brain development for males and females, which uniquely explains vulnerability to externalizing problems. The findings highlight the importance of examining sex-specific effects of adversity on adolescent development and mental health.

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Objective
The Adolescent Brain Cognitive DevelopmentSM (ABCD) Study, which follows over 11,000 adolescents, provides a unique opportunity to examine the causes and consequences of school detentions and suspensions. Although school records are considered the gold standard for assessing disciplinary events, they are not available in the ABCD Study®. Instead, youth and caregivers provide single-item reports of past-year discipline that may differ in scope and severity. The current study explored whether prospective associations with future school discipline varied by reporter, focusing on prior-year adolescent mental health concerns and discipline history as predictors.

Method
Data from the ABCD Study (baseline n = 9,772; 8-11 years old; 52% male) were analyzed using linear mixed-effects models with multiple imputation. Multi-informant mental health concerns (externalizing, inattention/impulsivity, and internalizing) from the first follow-up wave predicted discipline over the next two years across four discipline reporting groups: Youth-Reported (20%), Caregiver-Reported (13%), Agreement (10%), and Either Reporter (24%).

Results
Youth-reported and either-reporter discipline measures showed higher prevalence rates but weaker bivariate associations with prior mental health and disciplinary history relative to caregiver-reported and agreement discipline measures; however, most differences diminished after covariate adjustment. Across reporters, prior discipline remained the strongest predictor of future discipline.

Conclusion
Reporter choice in school discipline measurement influenced observed associations. Patterns suggested that youth-reported discipline may capture a broad range of infractions, whereas caregiver-reported discipline may reflect more severe events. However, recognizing the limited precision of single-item discipline indicators is essential for interpreting results and guiding future ABCD investigations.

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Because suicide-related outcome risk is higher among individuals experiencing adverse childhood experiences (ACEs), and individuals of minoritized race and ethnicity experience greater ACEs, differences by race and ethnicity in ACE exposure and/or response may help explain racial and ethnic disparities in suicide-related outcomes. We aimed to describe ACE prevalence by race and ethnicity, estimate associations between ACEs and suicidality, and explore moderation by race and ethnicity. Supported by the stress sensitization hypothesis, we hypothesized that associations between ACEs and suicidality would be stronger among non-Hispanic Black and Hispanic children than non-Hispanic White children. We utilized an Adolescent Brain Cognitive Development study subsample ( = 5,469; = 119.3 months [ = 7.5 months]; Hispanic: 20.8%; non-Hispanic Black: 14.8%; non-Hispanic White: 64.4%). We estimated associations between ACEs (cumulative ACE score and three subdomains: family-centered adversity, interpersonal adversity, and life events) and suicidality (any child-reported suicidal thoughts or behaviors) using generalized linear mixed models and included an interaction term between ACEs and race and ethnicity to examine potential moderation. ACE prevalence differed by race and ethnicity and was highest among non-Hispanic Black children, although household mental illness prevalence was highest among non-Hispanic White children. Cumulative ACE score ( = 1.17, 95% CI [1.12, 1.23]), family-centered adversity ( = 1.89, 95% CI [1.54, 2.32]), and interpersonal adversity ( = 1.62, 95% CI [1.35, 1.94]) were positively associated with suicidality; the associations were not moderated by race and ethnicity. Differential ACE exposure by race and ethnicity may help explain suicide-related disparities. ACE prevention and interventions, particularly among children of minoritized race and ethnicity, are vital. (PsycInfo Database Record (c) 2026 APA, all rights reserved).

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Background
Psychiatric disorders affect approximately 20% of adolescents in the U.S. and are both heritable and highly polygenic. Polygenic scores (PGSs) aggregate genetic risk across the genome, and in doing so potentially capture multiple, distinct behavioral pathways. Among these, cognitive control and reward sensitivity are key constructs that have been found to independently and jointly relate to adolescent psychopathology.

Methods
In this study, we used latent variables representing cognitive control and reward sensitivity (measured at baseline) as mediators between PGSs for internalizing, neurodevelopmental, and addiction-related psychopathology and observed psychopathology measured two years later in the Adolescent Brain Cognitive Development Study (N=11,875; ages 9–12; 48% female, 52% male assigned at birth).

Results
Our findings show that most of the associations between PGSs and later psychopathology were accounted for by indirect effects through cognitive control and reward sensitivity, with all of the association between the addiction PGS and Externalizing accounted for by the indirect effects, but less of the internalizing PGS to Internalizing pathway was accounted for by control and reward sensitivity. Multiple cognitive control factors significantly mediated the effects of PGSs on both internalizing and externalizing outcomes (indirect effects=0.004–0.074). Reward sensitivity, specifically Sensation Seeking, uniquely mediated the association between the addiction PGS and later psychopathology, suggesting that addiction-related genetic risk may operate through pathways related to heightened reward responsiveness.

Conclusions
Overall, these results indicate that PGSs for internalizing, neurodevelopmental, and addiction-related traits index multiple distinct behavioral mechanisms with specific relevance to adolescent psychopathology risk.

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Background
Childhood disruptive behavior problems are linked to aberrant integrity within large-scale cognitive control networks. However, it is unclear if transitory or dynamic variation in the functional brain architecture is a marker of disruptive behavior problems. The current study tested whether functional connectivity across dynamic networks is distinctly associated with the transdiagnostic symptom domain of disruptive behavior problems in children.

Methods
Participants were aged 9-10 years from the Adolescent Brain Cognitive Development (ABCD) Study, who completed resting-state fMRI (N=877). We employed a dynamic connectivity approach leveraging a hidden semi-Markov model (HSMM) to identify transient properties of brain networks and states. Models estimated the time spent in each state (occupancy time) and the number of consecutive timepoints in a state (dwell time) for each participant. Linear regression models were utilized to identify distinct associations between dynamic properties (occupancy and sojourn times) and severity of disruptive behavior problems, accounting for other commonly co-occurring symptoms.

Results
Dynamic network markers of disruptive behavior problems included increased time in network states characterized by globally aberrant connectivity patterns in circuitry involved in cognitive control including frontoparietal and dorsal attention networks. Reliability of findings was found in a held-out sample of resting-state fMRI runs in which greater severity of disruptive behavior problems was uniquely linked to greater occupancy time in similarly characterized brain states.

Conclusion
Transdiagnostic, dynamic resting-state markers of disruptive behavior problems in youth may assist in the development of brain-based biomarkers for monitoring treatment outcomes, assessing circuit target engagement and informing clinical decisions.

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Exposure to early life adversity has long-reaching effects on the psychopathology of adolescents. However, some individuals exposed to early life stressors, such as threat and deprivation, do not later present with symptoms. Previous research suggests that neural mechanisms may play a role in differentiating pathways from early life threat or deprivation to internalizing symptoms.

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Positive expectancies of cannabis use effects, which are the beliefs about the anticipated positive effects of cannabis, are robust cognitive precursors of adolescent cannabis initiation and escalation. However, little is known about how sociodemographic, familial, and psychopathological factors predict positive expectancies of cannabis use effects or how these expectancies evolve across early adolescence.

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The gateway hypothesis posits that the use of some “gateway drugs” may precipitate initiation of use of other drugs. A commonly examined pathway in this regard is the use of tobacco/nicotine leading to the use of marijuana. There is a dearth of research that has examined nicotine vaping specifically as a predictor of marijuana and that has integrated social learning processes of rule-breaking peer association into this pathway. The present study sought to address these gaps in the literature by examining nicotine vaping as a mediator of the relationship between rule-breaking peer association and marijuana use. The Adolescent Brain Cognitive Development data were analyzed. Generalized structural equation modeling was used to assess relationships of interest. Greater rule-breaking peer association predicted increased marijuana use risk at follow-up. Nicotine vaping was a significant mediator here, accounting for about 8% of this relationship. Implications are discussed.

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Despite the rise of adolescent video gaming, evidence-based parenting guidelines and research on its specific behavioral impacts remain limited. This study evaluated whether media parenting practices are prospectively associated with video game use in adolescents 1 and 2 years later.

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Objective
Greater peer victimization predicts more internalizing symptoms, particularly among adolescent girls. However, not all adolescents are equally sensitive to peer interactions; rostral anterior cingulate cortex (rACC) reactivity to social cues may mark these differences in sensitivity. rACC activation to social stimuli may mark individuals for whom peer victimization leads to internalizing symptoms; this effect may vary by sex and level of peer victimization. Understanding unique pathways to internalizing symptoms may provide increasing insight into heterogeneity of emerging internalizing symptoms as well as precision targets for intervention.

Method
Participants (n=1,557; ages 11-12) from the Adolescent Brain Cognitive Development (ABCD) study completed functional neuroimaging and questionnaires. Participants were divided into quartiles of rACC social activation (faces>places) during the Emotional N-back task.

Results
Higher quartiles of left, but not right, rACC social activation were associated with higher levels of internalizing symptoms (b=6.777e-02). In female participants, high rACC social activation related to decreased internalizing symptoms as victimization increased (b=-0.08) compared to female participants with average and low rACC social activation and all male participants.

Conclusion
Lateralized rACC social activation may mark sensitivity to internalizing symptoms and peer victimization. At normative-to-low levels of peer victimization, higher rACC social activation marked a particularly vulnerable group to peer victimization. However, in female participants higher rACC social activation may be protective against high peer victimization where it decreased the association between peer victimization and internalizing symptoms. The rACC may be a treatment target for to reduce internalizing symptoms, but social context is an important factor contributing to heterogeneity.

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Adverse prenatal exposures (APEs) often co-occur and independently associate with risk for childhood psychopathology. Whether exposure to multiple APEs is associated with persistent clinical effects through adolescence or underlying changes in brain maturation remains uncertain.

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To investigate sex-dependent effects of polygenic risk (PRS-SCZ) and exposome score (ES-SCZ) for schizophrenia, both independently and jointly, on distressing psychotic experiences (PEs) in early adolescents.

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