Background: Childhood disruptive behavior problems are linked to aberrant integrity within large-scale cognitive control networks. However, it is unclear whether transitory or dynamic variation in the functional brain architecture is a marker of disruptive behavior problems. In this study, we tested whether functional connectivity across dynamic networks is distinctly associated with the transdiagnostic symptom domain of disruptive behavior problems in children. Methods: Participants were 9 to 10-year-olds from the Adolescent Brain Cognitive Development Study who completed resting-state functional magnetic resonance imaging (fMRI) (N = 877). We used a dynamic connectivity approach leveraging a hidden semi-Markov model to identify transient properties of brain networks and states. Models estimated the time spent in each state (occupancy time) and the number of consecutive time points 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, while 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. Conclusions: 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.

Background: Dimensional models of early life adversity (ELA) posit distinct developmental consequences of threat, deprivation, uncontrollability, and unpredictability. Existing approaches force each event into a single dimension or rely on self-ratings that may conflate exposure with subjective appraisal. Objective: We evaluated norm-based dimensional ratings as an alternative and examined their associations with emotion regulation and psychopathology. Participants and Setting: A Prolific sample (N=200; Mage=23.06; 40.5% female; 48% racial minorities) was used to establish the norms; a community sample (N=291; Mage=22.40; 59.5% female; 60.5% racial minorities) was used to test the norms out of sample. Methods: In Sample 1, we developed norms from averaged ratings of 82 ELA items and compared norm-based and self-rating scoring (feasibility test). In Sample 2, we applied Sample 1 norms (replicability test). Dimension scores—threat, deprivation, unpredictability, uncontrollability—predicted cognitive reappraisal, emotion dysregulation, and psychopathology symptoms. Results: Although discrete events differed in dimensional profiles, cumulative person-level dimensional scores had high co-occurrence (VIFs>100). Norm-based and self-rating scoring produced comparable patterns in Sample 1, replicated in Sample 2. Entered simultaneously, deprivation was the dominant predictor of depression, PTSD, and emotion dysregulation across both samples (R2 = .04-.23, ps < .01) and the only dimension negatively associated with cognitive reappraisal (p = .007). Conclusions: ELA dimensions are entangled at the person level, preventing clean specificity in naturalistic samples, converging with recent concerns about event-based dimensional approaches. The value of dimensional models may inform sample selection, treat self–norm discrepancies as meaningful appraisal differences, and target such appraisals through interventions.

Intergenerational transmission of mental well-being and socioemotional functioning is widely documented at the behavioral level, yet how such patterns are instantiated in the brain remains poorly understood. Using a movie-watching fMRI paradigm, we investigated parent-child similarity in socioemotional processing and its associations with family environment, parental emotion regulation, and similarity in internalizing symptoms. Across 258 family members (120 children, 138 parents), parent–child dyads showed greater neural similarity in socioemotional processing than unrelated adult–child pairs. Effects were concentrated in prefrontal and temporal regions, particularly the right lateral prefrontal cortex (PFC). Neural similarity was stronger in mother–daughter and father–son dyads. Poorer family functioning was associated with reduced whole-brain similarity. Critically, parent-child right lateral PFC similarity was associated with similarity in internalizing symptoms depending on parental emotion regulation. These findings establish parent–child socioemotional neural similarity as a context-dependent pathway through which intergenerational patterns of mental well-being may emerge.

Background: Adolescence is a developmental period involving ongoing white matter (WM) maturation and rising risk for psychopathology. This risk is particularly elevated among youth whose parents have mental health problems. Methods: Leveraging longitudinal data from three waves of the community-based Adolescent Brain Cognitive Development (ABCD) Study (N = 6,581, Nobservations = 16, 271, mean ageTP 1 = 10.2, mean ageTP 2 = 12.0 , mean ageTP 3 = 14.2), we employed random intercept cross-lagged panel models (RI-CLPMs) to disentangle stable between-person differences from time-varying within-person changes. We examined prospective and bidirectional associations between youth general psychopathology and diffusion metrics, including fractional anisotropy (FA) and mean diffusivity (MD) in the uncinate fasciculus (UF), superior longitudinal fasciculus (SLF), and corpus callosum (CC). We also tested whether parental psychopathology moderated these associations. Results: Preregistered analyses showed no significant between-person or within-person associations between parent-reported youth psychopathology and WM microstructure, nor evidence of moderation by parental psychopathology. In exploratory analyses using youth self-reports, SLF and CC FA were negatively associated with psychopathology at the between-person level, but positively associated at the within-person level during early adolescence. Additionally, SLF and CC MD were negatively associated with self-reported psychopathology on the within-person level during early adolescence, with this association persisting into mid-adolescence for the CC. Parental psychopathology moderated the within-person association between CC MD and self-reported youth psychopathology. Conclusion: Overall, the findings did not support hypothesized prospective and bidirectional associations between parent-reported youth psychopathology and WM microstructure, nor moderation by parental psychopathology. Instead, our findings highlight limitations of tract-specific explanations for general psychopathology in at-risk youth, informant discrepancies, and the importance of separating between- and within-person effects.

Past traumatic experiences shape neural responses to future stress, but the mechanisms underlying this dynamic interaction remain unclear. Here, we assessed how trauma-related brain networks respond to current acute stress in real time. Using a machine learning approach, we trained and tested brain functional connectivity networks to predict past trauma exposure in a community sample of adults (N = 170). We then evaluated the response of these trauma-predictive brain networks to an acute emotional and physiological stressor in a subsample of participants (N = 92) and to a pharmacological manipulation (hydrocortisone) in an independent crossover study (N = 27). We found that connectome-based predictive modeling successfully predicted past trauma exposure. The network associated with greater trauma exposure showed high involvement of salience network connections, with model prediction driven by connectivity in the medial frontal cortex, salience network, motor regions, default mode network, and cerebellum. Notably, connectivity in this trauma-predictive network was significantly attenuated following an acute stressor relative to control. A similar pattern was observed in the pharmacology sample, with decreased connectivity under hydrocortisone compared to placebo within this trauma-predictive network. Finally, attenuated trauma-predictive network connectivity after acute stress was associated with lower depressive symptoms in the stress-exposed group, but not control group. These findings suggest that stress may induce blunted connectivity of brain networks related to past traumatic experiences and that the reduced engagement of these trauma-predictive brain networks may facilitate adaptive regulatory response to later stress.

Background: It is unclear how transdiagnostic symptoms including attention, disruptive behavior, and internalizing problems are linked to in-scanner motion in children across structural and functional magnetic resonance imaging (fMRI). In the current study, we examined whether transdiagnostic symptoms of attention, disruptive behavior, and internalizing problems were associated with scanner motion in children during multimodal imaging. Methods: In 9045 children ages 9 to 10 years in the ABCD (Adolescent Brain Cognitive Development) Study, logistic regression and linear mixed-effects models were used to examine associations between motion and behavior. Motion was indexed using ABCD Study quality control (QC) metrics and mean framewise displacement for T1- and T2-weighted structural, resting-state, and diffusion MRI; stop-signal task; monetary incentive delay task; and emotional n-back task. The Child Behavior Checklist was used as a continuous measure of symptom severity. Results: Greater severity of attention and disruptive behavior problems was associated with a lower likelihood of passing motion QC across imaging modalities, while increased internalizing severity was associated with a higher likelihood of passing. There was also an interaction between sex and attention-related problems in passing QC for T2-weighted and diffusion MRI scans. Increased attention and disruptive behavior problems were associated with increased mean motion, whereas increased internalizing problems were associated with decreased mean motion. Greater severity of attention problems was associated with worse performance across the fMRI tasks. Conclusions: These findings have implications for advancing the development of computational and behavioral approaches for mitigating motion effects in youths, enhancing accessibility of imaging protocols and representativeness influences across child psychiatric disorders, and identifying brain-based biomarkers.

Early adversity can alter the maturation and function of neural regions that support affective functioning, including threat and safety learning. A growing body of cross-species research has specifically focused on the role of unpredictability in childhood environments in shaping affective functioning; however, the links between childhood unpredictability and neural function related to extinction learning in adulthood remain unclear. In this study, we probed the association between childhood unpredictability, extinction learning, and neural activation in four regions implicated in extinction learning in healthy young adults (N = 45; aged 18-30 years). Results revealed that adults exposed to more unpredictable childhood environments showed greater basolateral amygdala activity to the former (i.e., extinguished) threat cue during early, but not late, extinction, including when controlling for current anxiety and childhood trauma exposure. An exploratory analysis showed that exposure to unpredictable caregiving, but not distal unpredictability (e.g., unpredictability of the physical home or community), specifically drove findings in the amygdala. Childhood unpredictability was not associated with activity in the other regions of interest or with skin conductance response during extinction. These findings add to a growing literature on longstanding impacts of unpredictable caregiving environments, with implications for promoting healthy neurodevelopment and targeted clinical interventions.

OBJECTIVE:Youth whose parents have depression histories are at elevated risk for psychopathology. Familial depression-related patterns of neurodevelopment and environmental stress (eg, family conflict) likely contribute to heightened risk. However, knowledge remains limited due to few studies, small sample sizes, and cross-sectional designs. We sought to identify how neural circuitry, familial risk for depression, and family conflict interact during preadolescence to predict adolescent psychopathology. METHOD:Participants included healthy (no lifetime psychiatric diagnoses) youth at high (HR, n = 794; at least one parent with a depression history) and low (LR, n = 1,708; no parental history of psychopathology) familial risk for depression, aged 9 to 10, from the Adolescent Brain Cognitive Development℠ (ABCD) Study. We tested whether functional connectivity (FC) among 12 resting-state networks interacted with risk status and family conflict at ages 9 to 10 to predict psychiatric symptoms at ages 12 to 13. RESULTS:Risk status significantly interacted with family conflict and cingulo-parietal network (CPN) FC at ages 9 to 10 to predict total problems and internalizing symptoms at ages 12 to 13 (R2 = 0.349, ΔR2 = 0.017, ηp2 = 0.005; R2 = 0.254, ΔR2 = 0.023, ηp2 = 0.004, respectively). Specifically, among youth in low (but not high) family conflict environments, there was a significant negative association between CPN FC at ages 9 to 10 and psychiatric symptoms at ages 12 to 13 for HR youth, whereas this association was significantly positive for LR youth. CONCLUSION:Findings suggest that CPN connectivity and family conflict in preadolescence may be prognostic risk markers for future symptoms related to parental depression. These markers may shed light on brain-based processes by which environmental adversity relates to heightened familial risk for psychopathology, although small effect sizes necessitate future investigation to better understand the potential clinical relevance. PLAIN LANGUAGE SUMMARY:This study followed over 2,500 children from ages 9 to 10 to examine how brain connectivity and family conflict relate to later mental health symptoms at the ages of 12 to 13 in youth with and without a parental history of depression. The authors found that connections in the cingulo-parietal brain network (CPN), together with levels of family conflict, predicted later emotional and behavioral problems differently for high‑risk (parent with depression) and low‑risk youth. In low‑conflict families, stronger connectivity in this network at ages 9 to 10 predicted fewer later symptoms for high‑risk youth, but more later symptoms for low‑risk youth. These findings suggest that being in a low family conflict environment may be protective, but its effects depend on brain connectivity and parental mental health.

Early-life adversity is pervasive worldwide and represents a potent risk factor for increased mental health burden across the lifespan. However, there is substantial individual heterogeneity in associations between adversity exposure, neurobiological changes, and mental health problems. Accounting for key features of adversity such as the developmental timing of exposure may clarify associations between adversity, neurodevelopment, and mental health. The present study leverages sparse canonical correlation analysis to characterize modes of covariation between age of adversity exposure and the integrity of white matter tracts throughout the brain in a sample of 107 adults. We find that adversity exposure during middle childhood (ages 5-6 and 8-9 in particular) is consistently linked with alterations in white matter tract integrity, such that tracts supporting sensorimotor functions display higher integrity in relation to adversity exposure while tracts supporting cortico-cortical communication display lower integrity. Further, latent patterns of tract integrity linked with adversity experienced across preschool age and middle childhood (ages 4-9) were associated with trauma-related symptoms in adulthood. Our findings underscore that adversity exposure may differentially affect white matter in a function- and developmental-timing specific manner and suggest that adversity experienced between ages 4-9 may shape the development of global white matter tracts in ways that are relevant for adult mental health.

PURPOSE:To assess longitudinal and geographic variation in perceived discrimination from ages 10-11 to 13-14 years in the Adolescent Brain Cognitive Development cohort, and to examine how these experiences are shaped by contextual factors such as neighborhood segregation and state-level racial bias. METHODS:Data were drawn from the longitudinal Adolescent Brain Cognitive Development Study (release 5.1), analyzing years 1, 2, and 4, corresponding to approximate ages 10-11, 11-12, and 13-14 years. Perceived discrimination was assessed using items adapted from the Perceived Discrimination Scale. Mixed-effects logistic regression models examined how perceived discrimination varied across time, demographic factors, and contextual variables, with models weighted using American Community Survey raked propensity scores to ensure national representativeness. RESULTS:Black, Asian American and Pacific Islander, and Other/Multiracial non-Hispanic youth showed increasing trajectories of perceived discrimination over time, while Native American and White non-Hispanic youth exhibited decreasing trends. Significant geographic variation emerged, with Black youth reporting elevated discrimination across all regions, particularly in the West and South. Youth living in areas with concentrated poor Black households and in states with high anti-Black bias reported higher discrimination. Youth with immigrant backgrounds generally reported higher levels of perceived discrimination across most racial/ethnic groups. DISCUSSION:Perceived discrimination follows distinct developmental trajectories during early adolescence that vary significantly by race, ethnicity, geography, and structural context. These findings highlight the critical need for targeted interventions during this developmental period, particularly for Black, Asian American and Pacific Islander, and Other/Multiracial youth. Context-specific approaches to addressing racism are essential for mitigating its harmful effects on adolescent development.

OBJECTIVE:Early-life stress (ELS) has been linked to the development of psychopathology-related outcomes, including posttraumatic stress symptoms (PTSS). Locus of control (LOC) is one factor thought to be critical to the development of PTSS. METHOD:The present study used latent profile analysis across two nonrepresentative samples (i.e., laboratory and online) of young adults (N = 164 and N = 665) to identify subgroups based on LOC orientation and PTSS severity and to explore early environmental correlates of individuals' membership in distinct subgroups. RESULTS:Across both samples, results of the latent profile analyses indicated a best fitting five-class solution. Cumulative ELS and perceived uncontrollability of ELS exposure emerged as significant predictors of subgroup membership in the Mechanical Turk sample. CONCLUSIONS:These findings suggest that associations between perceptions of control at the event (i.e., controllability during a stressful event) and global (i.e., LOC orientation) levels may play a role in the development of stress-related symptoms following ELS. (PsycInfo Database Record (c) 2025 APA, all rights reserved).

Parsing heterogeneity in the nature of adversity exposure and neurobiological functioning may facilitate better understanding of how adversity shapes individual variation in risk for and resilience against anxiety. One putative mechanism linking adversity exposure with anxiety is disrupted threat and safety learning. Here, we applied a person-centered approach (latent profile analysis) to characterize patterns of adversity exposure at specific developmental stages and threat/safety discrimination in corticolimbic circuitry in 120 young adults. We then compared how the resultant profiles differed in anxiety symptoms. Three latent profiles emerged: (1) a group with lower lifetime adversity, higher neural activation to threat, and lower neural activation to safety; (2) a group with moderate adversity during middle childhood and adolescence, lower neural activation to threat, and higher neural activation to safety; and (3) a group with higher lifetime adversity exposure and minimal neural activation to both threat and safety. Individuals in the second profile had lower anxiety than the other profiles. These findings demonstrate how variability in within-person combinations of adversity exposure and neural threat/safety discrimination can differentially relate to anxiety, and suggest that for some individuals, moderate adversity exposure during middle childhood and adolescence could be associated with processes that foster resilience to future anxiety.

Background: Altered gaze in social settings is a hallmark of social anxiety; however, little research directly examines gaze in anxiety-provoking contexts among youth with anxiety disorders, limiting mechanistic insight into pediatric anxiety. The present study leveraged mobile eye-tracking technology to examine gaze behavior during a naturalistic stressor in a clinical developmental sample. Methods: Sixty-one youth (ages 8-17 years; 28 with anxiety disorders, 33 non-anxious controls) completed a naturalistic social stress task (public speaking in front of a videotaped classroom audience) while wearing eyetracking glasses. Gaze behavior and state anxiety were quantified in each group during two task conditions: while giving a speech and while passively viewing the audience. Results: Anxiety-related differences emerged in state anxiety and gaze behavior. First, a significant interaction between diagnostic group and task condition on state anxiety indicated that while anxiety increased among nonanxious controls following the speech, youth with anxiety disorders reported persistently elevated anxiety across all assessments. Second, a significant interaction emerged between social anxiety symptom severity and task condition on gaze time on the audience. While youth overall showed low dwell time on the audience during speech delivery, individuals with greater social anxiety showed longer gaze on the audience during the passive viewing condition. This pattern was specific to dimensional analyses of social anxiety symptom severity. Limitations: The current study was not sufficiently powered to examine age-related differences. Conclusions: These findings highlight anxiety-related differences in gaze behavior in youth, providing new mechanistic insight into pediatric anxiety using mobile eye-tracking.

Objective: Nearly 65% of youth experience trauma, and up to one-third of youth with trauma exposure face profound mental health sequelae. There remains a need to elucidate factors that contribute to psychopathology following trauma exposure, and to optimize interventions for youth who do not benefit sufficiently from existing treatments. Here, we probe safety signal learning (SSL), which is a mechanism of fear reduction that leverages learned safety to inhibit fear in the presence of threat-associated stimuli and has been shown to attenuate fear via a hippocampal-cingulate--specifically, a dorsal anterior cingulate cortex (dACC)--pathway. Method: The present study used behavioral and task-based functional magnetic resonance imaging data to examine age-related associations between interpersonal trauma exposure and the behavioral and neural correlates (ie, activation and functional connectivity) of SSL in a group of 102 youth (aged 9-19 years; 46 female, 56 male) with (n = 52) and without (n = 50) interpersonal trauma exposure. Primary analyses examined anterior hippocampal activation and anterior hippocampus-dACC functional connectivity. Exploratory analyses examined centromedial amygdala (CMA) and laterobasal amygdala (LBA) activation and anterior hippocampal, CMA, and LBA functional connectivity with additional anterior cingulate subregions (ie, subgenual anterior cingulate cortex [sgACC] and rostral anterior cingulate cortex [rosACC]). Results: Both youth with and without interpersonal trauma exposure successfully learned conditioned safety, which was determined by using self-report of contingency awareness. Youth with interpersonal trauma exposure (relative to youth in the comparison group) exhibited age-specific patterns of lower hippocampal activation (F2,96 = 3.75, PFDR = .049, hp2 = 0.072), and, in exploratory analyses, showed heightened centromedial amygdala activation (F1,96 = 5.37, PFDR = .046, hp2 = 0.053) and an age-related decrease in hippocampal-sgACC functional connectivity during SSL (F1,94 = 10.68, PFDR = .015, hp2 = 0.102). We also show that hippocampal-sgACC functional connectivity mediated the association between interpersonal trauma exposure and post-traumatic stress disorder symptoms in an age-specific manner in the overall sample. Conclusion: Together, these findings suggest that although age-and trauma-specific differences in the neural correlates of SSL may relate to the development of psychopathology, youth with interpersonal trauma exposure demonstrate successful learning of conditioned safety over time. Plain language summary: Childhood trauma is a major risk factor for the development of psychiatric conditions such as posttraumatic stress disorder (PTSD). Using cross-sectional analysis, this study examined age-related differences in safety signal learning and its neural correlates among youth (N=102) ages 9 to 19 with and without exposure to interpersonal trauma. The authors found that youth exposed to trauma successfully learned about cues signaling safety; however, they showed age-related differences in hippocampal-frontoamygdala circuitry during safety signal learning that might relate to risk for PTSD at specific developmental stages. These findings can inform efforts to promote safety learning and optimize developmentally focused interventions for youth with PTSD. Diversity & Inclusion Statement: We worked to ensure that the study questionnaires were prepared in an inclusive way. We worked to ensure sex and gender balance in the recruitment of human participants. We worked to ensure race, ethnic, and/or other types of diversity in the recruitment of human participants. While citing references scientifically relevant for this work, we also actively worked to promote sex and gender balance in our reference list. While citing references scientifically relevant for this work, we also actively worked to promote inclusion of historically underrepresented racial and/or ethnic groups in science in our reference list. We actively worked to promote sex and gender balance in our author group. We actively worked to promote inclusion of historically underrepresented racial and/or ethnic groups in science in our author group. One or more of the authors of this paper self-identifies as a member of one or more historically underrepresented racial and/or ethnic groups in science. One or more of the authors of this paper received support from a program designed to increase minority representation in science.

Neural variability, or variation in brain signals, facilitates dynamic brain responses to ongoing demands. This flexibility is important during development from childhood to young adulthood, a period characterized by rapid changes in experience. However, little is known about how variability in moment-to-moment brain state engagement changes during development. Such investigations would require the continuous assessment of multiple brain states concurrently. Here, we leverage a new computational framework to characterize the state engagement variability (SEV) developmental trajectory. A consistent pattern of SEV changing with age is identified across cross-sectional and longitudinal datasets (N > 3,000). The SEV developmental trajectory stabilizes around mid-adolescence, with timing varying by sex and brain state. SEV successfully predicts executive function (EF) in youth from an independent dataset. Deviations in SEV development are further linked to worse EF. These converging findings suggest that SEV changes over development, allowing individuals to flexibly recruit various brain states to meet evolving needs.