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One in three children in the United States is exposed to insecure housing conditions, including unaffordable, inconsistent, and unsafe housing. These exposures have detrimental impacts on youth mental health. Delineating the neurobehavioral pathways linking exposure to housing insecurity with children’s mental health has the potential to inform interventions and policy. However, in approaching this work, carefully considering the lived experiences of youth and families is essential to translating scientific discovery to improve health outcomes in an equitable and representative way. In the current paper, we provide an introduction to the range of stressful experiences that children may face when exposed to insecure housing conditions. Next, we highlight findings from the early-life stress literature regarding the potential neurobehavioral consequences of insecure housing, focusing on how unpredictability is associated with the neural circuitry supporting cognitive and emotional development. We then delineate how community-engaged research (CEnR) approaches have been leveraged to understand the effects of housing insecurity on mental health, and we propose future research directions that integrate developmental neuroscience research and CEnR approaches to maximize the impact of this work. We conclude by outlining practice and policy recommendations that aim to improve the mental health of children exposed to insecure housing.

Background: There is an imminent need to identify neural markers during preadolescence that are linked to developing depression during adolescence, especially among youth at elevated familial risk. However, longitudinal studies remain scarce and exhibit mixed findings. Here we aimed to elucidate functional connectivity (FC) patterns among preadolescents that interact with familial depression risk to predict depression two years later. Methods: 9–10 year-olds in the Adolescent Brain Cognitive Development (ABCD) Study were classified as healthy (i.e., no lifetime psychiatric diagnoses) at high familial risk for depression (HR; n=559) or at low familial risk for psychopathology (LR; n=1203). Whole-brain seed-to-voxel resting-state FC patterns with the amygdala, putamen, nucleus accumbens, and caudate were calculated. Multi-level, mixed-effects regression analyses were conducted to test whether FC at ages 9–10 interacted with familial risk to predict depression symptoms at ages 11–12. Results: HR youth demonstrated stronger associations between preadolescent FC and adolescent depression symptoms (ps0.001), primarily among amygdala/striatal FC with visual and sensory/somatomotor networks. Conclusions: Preadolescent amygdala and striatal FC may be useful biomarkers of adolescent-onset depression, particularly for youth with family histories of depression. This research may point to neurobiologically-informed approaches to prevention and intervention for depression in adolescents.

An extensive literature shows that race information can impact cognitive performance. Two key findings include an attentional bias to Black racial cues in U.S. samples and diminished recognition of other-race faces compared to same-race faces in predominantly White adult samples. Yet face stimuli are increasingly used in psychological research often unrelated to race (Conley et al., 2018) or without consideration for how race information may influence cognitive performance, especially among developmental participants from different racial groups. In the current study we used open-access data from the Adolescent Brain Cognitive DevelopmentSM (ABCD) Study® 4.0.1 release to test for developmentally similar other- and same-race effects of Black and White face stimuli on attention, working memory, and recognition memory in 9- and 10-year-old Black and White children (n=5,659) living in the U.S. Black and White children showed better performance when attending to Black versus White faces. We also show an advantage in recognition memory of same-race compared to other-race faces in White children that did not generalize to Black children. Together the findings highlight how race information, even when irrelevant to an experiment, may indirectly lead to misinterpretation of group differences in cognitive performance in children of different racial backgrounds.

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

Exposure to trauma throughout the lifespan is prevalent and increases the likelihood for the development of mental health conditions such as anxiety and post-traumatic stress disorder (PTSD). Safety signal learning (SSL)––a form of conditioned inhibition that involves reducing fear via conditioned safety––has been shown to effectively attenuate fear responses among individuals with trauma exposure, but the association between trauma exposure and the neural mechanisms of SSL remains unknown. Adults with varied prior exposure to trauma completed a conditioned inhibition task during functional MRI scanning and collection of skin conductance response (SCR). Conditioned safety signals reduced psychophysiological reactivity (i.e., SCR) in the overall sample. Although exposure to a higher number of traumatic events was associated with elevated SCR across all task conditions, SCR did not differ between threat in the presence of conditioned safety (i.e., SSL) relative to threat alone in a trauma-related manner. At the neural level, however, higher levels of trauma exposure were associated with lower hippocampal, amygdala, and dorsolateral prefrontal cortical activation during SSL. These findings suggest that while conditioned safety signals can reduce fear in the presence of threat even among individuals exposed to higher degrees of trauma, the neural circuitry involved in SSL is in fact sensitive to trauma exposure. Future research investigating neural processes during SSL among individuals with PTSD or anxiety can further elucidate the ways in which SSL and its neural correlates may reduce fear and link trauma exposure with later mental health conditions.

Adversity exposure is a risk factor for psychopathology, which most frequently onsets during adolescence, and prior research has demonstrated that alterations in cortico-limbic connectivity may account in part for this association. In a sample of youth from the Adolescent Brain Cognitive Development (ABCD) Study (N = 4006), we tested a longitudinal structural equation model to examine the indirect effect of adversity exposure (negative life events) on later psychopathology via changes in cortico-limbic resting-state functional connectivity (rsFC). We also examined the potential protective effects of parental acceptance. Generally, cortico-limbic connectivity became more strongly negative between baseline and year 2 follow-up, suggesting that stronger negative correlations within these cortico-limbic networks may reflect a more mature phenotype. Exposure to a greater number of negative life events was associated with stronger negative cortico-limbic rsFC which, in turn, was associated with lower internalizing (but not externalizing) symptoms. The indirect effect of negative life events on internalizing symptoms via cortico-limbic rsFC was significant. Parental acceptance did not moderate the association between negative life events and rsFC. Our findings highlight how stressful childhood experiences may accelerate neurobiological maturation in specific cortico-limbic connections, potentially reflecting an adaptive process that protects against internalizing problems in the context of adversity.

The Adolescent Brain Cognitive Development (ABCD) Study of 11,880 youth incorporates a comprehensive range of measures assessing predictors and outcomes related to mental health across childhood and adolescence in participating youth, as well as information about family mental health history. We have previously described the logic and content of the mental health assessment battery at Baseline and 1-year follow-up. Here, we describe changes to that battery and issues and clarifications that have emerged, as well as additions to the mental health battery at the 2-, 3-, 4-, and 5-year follow-ups. We capitalize on the recent release of longitudinal data for caregiver and youth report of mental health data to evaluate trajectories of dimensions of psychopathology as a function of demographic factors. For both caregiver and self-reported mental health symptoms, males showed age-related decreases in internalizing and externalizing symptoms, while females showed an increase in internalizing symptoms with age. Multiple indicators of socioeconomic status (caregiver education, family income, financial adversity, neighborhood poverty) accounted for unique variance in both caregiver and youth-reported externalizing and internalizing symptoms. These data highlight the importance of examining developmental trajectories of mental health as a function of key factors such as sex and socioeconomic environment.

Anxiety disorders are the most prevalent psychiatric condition among youth, with symptoms commonly emerging prior to or during adolescence. Delineating neurodevelopmental trajectories associated with anxiety disorders is important for understanding the pathophysiology of pediatric anxiety and for early risk identification. While a growing literature has yielded valuable insights into the nature of brain structure and function in pediatric anxiety, progress has been limited by inconsistent findings and challenges common to neuroimaging research. In this review, we first discuss these challenges and the promise of ‘big data’ to map neurodevelopmental trajectories in pediatric anxiety. Next, we review evidence of age-related differences in neural structure and function among anxious youth, with a focus on anxiety-relevant processes such as threat and safety learning. We then highlight large-scale cross-sectional and longitudinal studies that assess anxiety and are well positioned to inform our understanding of neurodevelopment in pediatric anxiety. Finally, we detail relevant challenges of ‘big data’ and propose future directions through which large publicly available datasets can advance knowledge of deviations from normative brain development in anxiety. Leveraging ‘big data’ will be essential for continued progress in understanding the neurobiology of pediatric anxiety, with implications for identifying markers of risk and novel treatment targets.

Childhood experiences play a profound role in conferring risk and resilience for brain and behavioral development. However, how different facets of the environment shape neurodevelopment remains largely unknown. Here we sought to decompose heterogeneous relationships between environmental factors and brain structure in 989 school-aged children from the Adolescent Brain Cognitive Development Study. We applied a cross-modal integration and clustering approach called ‘Similarity Network Fusion’, which combined two brain morphometrics (i.e., cortical thickness and myelin-surrogate markers), and key environmental factors (i.e., trauma exposure, neighborhood safety, school environment, and family environment) to identify homogeneous subtypes. Depending on the subtyping resolution, results identified two or five subgroups, each characterized by distinct brain structure–environment profiles. Notably, more supportive caregiving and school environments were associated with greater myelination, whereas less supportive caregiving, higher family conflict and psychopathology, and higher perceived neighborhood safety were observed with greater cortical thickness. These subtypes were highly reproducible and predicted externalizing symptoms and overall mental health problems. Our findings support the theory that distinct environmental exposures are differentially associated with alterations in structural neurodevelopment. Delineating more precise associations between risk factors, protective factors, and brain development may inform approaches to enhance risk identification and optimize interventions targeting specific experiences.

Although decades of research have shown associations between early caregiving adversity, stress physiology and limbic brain volume (e.g., amygdala, hippocampus), the developmental trajectories of these phenotypes are not well characterized. In the current study, we used an accelerated longitudinal design to assess the development of stress physiology, amygdala, and hippocampal volume following early institutional care. Previously Institutionalized (PI; N = 93) and comparison (COMP; N = 161) youth (ages 4–20 years old) completed 1–3 waves of data collection, each spaced approximately 2 years apart, for diurnal cortisol (N = 239) and structural MRI (N = 156). We observed a developmental shift in morning cortisol in the PI group, with blunted levels in childhood and heightened levels in late adolescence. PI history was associated with reduced hippocampal volume and reduced growth rate of the amygdala, resulting in smaller volumes by adolescence. Amygdala and hippocampal volumes were also prospectively associated with future morning cortisol in both groups. These results indicate that adversity-related physiological and neural phenotypes are not stationary during development but instead exhibit dynamic and interdependent changes from early childhood to early adulthood.

Several studies have shown that young children who have experienced early caregiving adversity (e.g. previously institutionalization (PI)) exhibit flattened diurnal cortisol slopes; however, less is known about how these patterns might differ between children and adolescents, since the transition between childhood and adolescence is a time of purported plasticity in the hypothalamic-pituitary-adrenal (HPA) axis. PI youth experience a massive improvement in caregiving environment once adopted into families; therefore we anticipated that a developmental increase in HPA axis plasticity during adolescence might additionally allow for an enhanced enrichment effect by the adoptive family. In a cross-sectional sample of 197 youths (PI and Comparison; 4–15 years old) we observed age-related group differences in diurnal slope. First replicating previous findings, PI children exhibited flattened diurnal slope. This group difference, however, was not observed in adolescents. Moderation analyses showed that pubertal development, increased time with family, and early adoption contributed to the steeper diurnal cortisol slope in PI adolescents. These findings add support to existing theories positing that the transition between middle childhood and adolescence may mark an additional sensitive period for diurnal cortisol patterning, allowing PI youth to benefit from the enriched environment provided by adoptive parents during this period of development. Keywords: Childhood, Adolescence, Stress, Enrichment, Early adversity

Functional connectivity (FC) between the amygdala and the ventromedial prefrontal cortex underlies socioemotional functioning, a core domain of impairment in autism spectrum disorder (ASD). Although frontoamygdala circuitry undergoes dynamic changes throughout development, little is known about age-related changes in frontoamygdala networks in ASD. Here we characterize frontoamygdala resting-state FC in a cross-sectional sample (ages 7–25) of 58 typically developing (TD) individuals and 53 individuals with ASD. Contrary to hypotheses, individuals with ASD did not show different age-related patterns of frontoamygdala FC compared with TD individuals. However, overall group differences in frontoamygdala FC were observed. Specifically, relative to TD individuals, individuals with ASD showed weaker frontoamygdala FC between the right basolateral (BL) amygdala and the rostral anterior cingulate cortex (rACC). These findings extend prior work to a broader developmental range in ASD, and indicate ASD-related differences in frontoamygdala FC that may underlie core socioemotional impairments in children and adolescents with ASD. Keywords: Autism spectrum disorder (ASD), Amygdala, Development, Resting-state functional connectivity, Adolescence, Prefrontal cortex

Stress can have lasting effects on the brain and behavior. Delineating the impact of stress on the developing brain is fundamental for understanding mechanisms through which stress induces persistent effects on behavior that can lead to psychopathology. The growing field of translational developmental neuroscience has revealed a significant role of the timing of stress on risk, resilience, and neuroplasticity. Studies of stress across species have provided essential insight into the mechanisms by which the brain changes and the timing of those changes on outcome. In this article, we review the neurobiological effects of stress and propose a model by which sensitive periods of neural development interact with stressful life events to affect plasticity and the effects of stress on functional outcomes. We then highlight how early-life stress can alter the course of brain development. Finally, we examine mechanisms of buffering against early-life stress that may promote resilience and positive outcomes. The findings are discussed in the context of implications for early identification of risk and resilience factors and development of novel interventions that target the biological state of the developing brain to ultimately ameliorate the adverse consequences of stress during childhood and adolescence.