Recent theories suggest that for youth highly sensitive to incentives, perceiving more social threat may contribute to social anxiety (SA) symptoms. In 129 girls (ages 11–13) oversampled for shy/fearful temperament, we thus examined how interactions between neural responses to social reward (vs. neutral) cues (measured during anticipation of peer feedback) and perceived social threat in daily peer interactions (measured using ecological momentary assessment) predict SA symptoms two years later. No significant interactions emerged when neural reward function was modeled as a latent factor. Secondary analyses showed that higher perceived social threat was associated with more severe SA symptoms two years later only for girls with higher basolateral amygdala (BLA) activation to social reward cues at baseline. Interaction effects were specific to BLA activation to social reward (not threat) cues, though a main effect of BLA activation to social threat (vs. neutral) cues on SA emerged. Unexpectedly, interactions between social threat and BLA activation to social reward cues also predicted generalized anxiety and depression symptoms two years later, suggesting possible transdiagnostic risk pathways. Perceiving high social threat may be particularly detrimental for youth highly sensitive to reward incentives, potentially due to mediating reward learning processes, though this remains to be tested.

This commentary discusses opportunities for advancing the field of developmental psychopathology through the integration of data science and neuroscience approaches. We first review elements of our research program investigating how early life adversity shapes neurodevelopment and may convey risk for psychopathology. We then illustrate three ways that data science techniques (e.g., machine learning) can support developmental psychopathology research, such as by distinguishing between common and diverse developmental outcomes after stress exposure. Finally, we discuss logistical and conceptual refinements that may aid the field moving forward. Throughout the piece, we underscore the profound impact of Dr Dante Cicchetti, reflecting on how his work influenced our own, and gave rise to the field of developmental psychopathology.

Understanding how youth perceive household economic hardship and how it relates to their behavior is vital given associations between hardship and behavioral development. Yet, most studies ignore youth’s own perceptions of economic hardship, instead relying solely on caregiver reports. Moreover, the literature has tended to treat economic hardship as a stable force over time, rather than a volatile one that varies month-to-month. This study addressed extant limitations by collecting monthly measures of economic hardship, specifically caregiver- and youth-reported material deprivation and youth-reported financial stress, and youth internalizing and externalizing problems from 104 youth–caregiver dyads (youth: 14–16 years, 55% female, 37% Black, 43% White) over nine months. We examined month-to-month variability of these constructs and how youth-reports of material deprivation and financial stress predicted their behavior problems, controlling for caregiver-reports of material deprivation. We found that hardship measures varied month-to-month (ICCs = 0.69–0.73), and youth-reported material deprivation positively predicted internalizing when examining both within- and between-individual variability (β = .19–.47). Youth-reported financial stress positively predicted within-individual variation in externalizing (β = .18), while youth reports of material deprivation predicted externalizing when looking between families (β = .41). Caregiver-reported material deprivation was unrelated to youth behavior when accounting for youth perceptions of economic hardship.

Twenty-six percent of children experience a traumatic event by the age of 4. Negative events during childhood have deleterious correlates later in life, including antisocial behavior. However, the mechanisms that play into this relation are unclear. We explored deficits in neurocognitive functioning, specifically problems in passive avoidance, a construct with elements of inhibitory control and learning as a potential acquired mediator for the pathway between cumulative early childhood adversity from birth to age 7 and later antisocial behavior through age 18, using prospective longitudinal data from 585 participants. Path analyses showed that cumulative early childhood adversity predicted impaired passive avoidance during adolescence and increased antisocial behavior during late adolescence. Furthermore, poor neurocognition, namely, passive avoidance, predicted later antisocial behavior and significantly mediated the relation between cumulative early childhood adversity and later antisocial behavior. This research has implications for understanding the development of later antisocial behavior and points to a potential target for neurocognitive intervention within the pathway from cumulative early childhood adversity to later antisocial behavior.

While child poverty is a significant risk factor for poor mental health, the developmental pathways involved with these associations are poorly understood. To advance knowledge about these important linkages, the present study examined the developmental sequelae of childhood exposure to poverty in a multiyear longitudinal study. Here, we focused on exposure to poverty, neurobiological circuitry connected to emotion dysregulation, later exposure to stressful life events, and symptoms of psychopathology. We grounded our work in a biopsychosocial perspective, with a specific interest in “stress sensitization” and emotion dysregulation. Motivated by past work, we first tested whether exposure to poverty was related to changes in the resting-state coupling between two brain structures centrally involved with emotion processing and regulation (the amygdala and the ventromedial prefrontal cortex; vmPFC). As predicted, we found lower household income at age 10 was related to lower resting-state coupling between these areas at age 15. We then tested if variations in amygdala–vmPFC connectivity interacted with more contemporaneous stressors to predict challenges with mental health at age 16. In line with past reports showing risk for poor mental health is greatest in those exposed to early and then later, more contemporaneous stress, we predicted and found that lower vmPFC–amygdala coupling in the context of greater contemporaneous stress was related to higher levels of internalizing and externalizing symptoms. We believe these important interactions between neurobiology and life history are an additional vantage point for understanding risk and resiliency, and suggest avenues for prediction of psychopathology related to early life challenge.

The experience of child maltreatment is a significant risk factor for the development of later internalizing disorders such as depression and anxiety. This risk is particularly heightened after exposure to additional, more contemporaneous stress. While behavioral evidence exists for such “stress sensitization,” little is known about the mechanisms mediating such relationships, particularly within the brain. Here we report that the experience of child maltreatment independent of recent life stress, gender, and age is associated with reduced structural integrity of the uncinate fasciculus, a major white matter pathway between the amygdala and ventromedial prefrontal cortex, in young adults. We further demonstrate that individuals with lower uncinate fasciculus integrity at baseline who subsequently experience stressful life events report higher levels of internalizing symptomatology at follow-up. Our findings suggest a novel neurobiological mechanism linking child maltreatment with later internalizing symptoms, specifically altered structural connectivity within the brain's threat-detection and emotion-regulation circuitry.