UCLA

Previous institutionalization (PI) is a potent stressor for the human infant. Such early stress can have long-lasting effects on emotional development (e.g., depression) and associated neurobiology. However the mechanisms underlying how early-life adversity (EA) increase neurobiological risk for depression are not fully understood. In this dissertation, I use a multi- method program of research, including experimental tasks, questionnaires, functional magnetic resonance imaging (fMRI), and epigenetic measures, to examine the developmental course of depression related phenotypes, as well as potential epigenetic and neurobiological mechanisms of this association. I further examined a potential behavioral intervention that may ameliorate depressive outcomes following EA. Study 1 shows that the nucleus accumbens (NAcc), a limbic structure associated with reward learning and motivation demonstrates atypical functioning following EA, specifically hypoactivity during the adolescent period, Study 2 shows that PI youth display blunted telomeres, DNA–protein complexes located at the end of chromosomes that protect from deterioration, which in concert with NAcc hypoactivity, predict depressive outcomes. Study 3 presents evidence suggesting that high levels of physical activity (PA) may predict decreases in depressive symptoms following EA. The results from the current study have important implications for understanding the associations between EA and both neural and genetic changes that may influence later depressive outcomes, and also provide a potential behavioral intervention by which these outcomes may be improved. Investigation of these associations in a developmental population is paramount, as early childhood may represent a critical period for the interaction between adversity, cellular aging, and neurodevelopment and thus highlights the significance of early intervention.