Exposure to stressful life events (SLEs) is involved in the etiology of most forms of psychopathology, and SLEs occurring early in development are particularly strong predictors of mental health problems. Most adolescent disorder onsets are temporally preceded by a major SLE. Yet, the mechanisms linking SLEs to the onset of adolescent psychopathology remain poorly understood. Prior research on mechanisms linking SLEs with youth mental disorders has focused largely on severe forms of adversity like abuse, neglect, and institutionalization. It is unknown whether similar mechanisms are involved in the link between less severe SLEs and psychopathology. Perhaps more critically, existing work has relied largely on cross-sectional between-subjects designs that compare children with exposure to some type of SLE to children without that experience. There is a dearth of longitudinal studies examining how SLEs influence emotion, cognition, behavior, and neural circuits within-individuals over time in ways that predict the emergence of psychopathology. The proposed research addresses this gap, using a novel methodological approach that permits examination of dynamic changes in emotion, cognition, social behavior, and neural function and connectivity following SLEs at a sufficiently fine grained level of temporal specificity to identify mechanisms underlying the link between SLEs and adolescent psychopathology as they unfold in real time. Specifically, the project will examine how monthly fluctuations in exposure to SLEs within-individuals predict subsequent changes in emotional processing in the Negative and Positive Valence Systems, Cognitive Control, Social Processes, and neural function and connectivity over a 12-month period. In addition to monthly assessments of SLEs, psychopathology, and potential mechanisms, passive monitoring of activity, sleep, and social behavior (e.g., interaction with peers through text and social media) through smartphones and wearable devices will allow additional mechanisms to be assessed passively and without subject burden. The study will investigate whether monthly variation in these emotional, cognitive, social, and neural processes predicts later increases in internalizing and externalizing problems in an accelerated cohort design with monthly assessments spanning age 11-18 years, producing 1,680 monthly observations over the study period. The longitudinal design and high-frequency assessments are innovative in allowing the identification of mechanisms that are altered by SLEs and prospectively predict psychopathology with high temporal specificity during a developmental period associated with increases in SLE exposure, stress vulnerability, and risk for psychopathology. Study findings will provide critical information regarding the specific domains of emotion, cognition, social behavior, and neural function that are altered by exposure to SLEs and increase vulnerability to psychopathology. These mechanisms represent modifiable targets for interventions to prevent the onset of stress-related psychopathology in children and adolescents.
The proposed research examines neurodevelopmental mechanisms underlying the powerful association of stressful life events (SLEs) with internalizing and externalizing psychopathology during adolescence. We use a novel methodological approach that permits examination of dynamic changes in emotion, cognition, social behavior, and neural function and connectivity following SLEs at a sufficiently fine grained level of temporal specificity to identify mechanisms underlying the link between SLEs and adolescent psychopathology as they unfold in real time. Elucidating these mechanisms will not only build knowledge of how environmental experience shapes development in ways that increase risk for psychopathology, but will also suggest possible targets for interventions to prevent the onset of stress-related psychopathology in children and adolescents.
