Neurodevelopmental Pathways to Depression in Adolescence: Socioeconomic Status, Cortical Structure, and Depression Symptoms

Abstract

Socioeconomic status (SES) is a key predictor of a multitude of health and functional outcomes, and growing up in low SES contexts is associated with poor neurocognitive outcomes and mental health problems across the lifespan. Recent studies of the links between SES and brain development suggest that associations between low SES and poor neurocognitive and health outcomes are likely accounted for by impacts on neurodevelopment. Low SES is associated with structural brain development, including reduced cortical thickness in frontal regions relevant to higher-level cognitive functions. However, understanding of how the impacts of SES on neurodevelopment contribute to developing psychopathology is limited. The study of how neurodevelopmental processes may contribute to depression is of particular interest given numerous neural correlates of depression, including reduced cortical thickness in frontal regions. Whereas both SES and depression independently have demonstrated associations with grey matter maturation, no studies to date have examined how the associations between SES, depression, and cortical structure interrelate. The current study addresses this gap in the literature by examining associations between SES at both household and neighborhood levels, depression symptoms, and cortical structure in adolescence. Furthermore, exploratory analyses investigated specific pathways of SES effects on depression symptoms and cortical structure through exposure to psychosocial stress. Data were drawn from an ongoing prospective longitudinal study of reward function development. Participants included 232 youth ages 9-13 (57.03% female; 46.59% White, 39.36% African American, 11.24% Multiracial, 2.81% Other; 11.24% Hispanic) and their primary caregivers who completed assessments of depression symptoms and stress at baseline and a 9-month follow-up, as well as an MRI assessment between baseline and follow up. Regression analyses examined associations between 1) SES to cortical structure, 2) SES to depression symptoms, 3) baseline depression symptoms and cortical structure, and 4) cortical structure to depression symptoms at follow-up. Structural equation models examined indirect effects of 1) SES on depression symptoms through cortical structure, 2) SES on cortical structure through depression symptoms, and 3) SES on cortical structure and depression symptoms through experiences of psychosocial stress. Neighborhood SES was positively associated with mean cortical thickness, and household SES was inversely associated with depression symptoms at follow up, controlling for baseline symptoms. No indirect effects were identified. Findings suggest that different aspects of SES may confer unique risks for neural and psychosocial development in early adolescence, such that SES of the neighborhood appears to have global effects on neurodevelopment that are not mediated by mood or proximal stress, whereas SES of the household appears to be associated with increasing mood symptoms and heightened stress experiences in early adolescence.