UCLA

Psychotic disorders disproportionately affect racial and ethnic minority groups, and prior research has shown that experiences of racial/ethnic discrimination can worsen symptoms and increase risk of developing psychotic disorders. However, psychological and biological mechanisms linking discrimination and psychosis have not been thoroughly explored. Further, while psychotic disorders are recognized as neurodevelopmental, there has been an absence of studies investigating how development interacts with discrimination and psychosis risk.The social defeat hypothesis offers a potential mechanism to understand the link between discrimination and psychosis risk. It suggests that social disadvantage or acute social stress can increase dopamine signaling in the brain's striatum, a neural marker associated with psychosis. Human studies have shown altered dopamine function in the striatum can impact connectivity of the striatum and large-scale cortical networks, which has implications for experiences of discrimination and patterns of functional connectivity observed in schizophrenia. Behaviorally, social defeat stress and altered dopamine function are linked to cognitive impairments and emotional disturbances, which in turn may elevate the risk of psychosis. In the transition from childhood to adulthood, functional brain networks undergo significant maturation. Relative to young adults, adolescents show greater subcortical activation to social stressors. Further, stressors in adolescence have longer-lasting effects on the brain relative to those in adulthood. These patterns may be due to changes in the striatal DA system during adolescence. Maturation of striatal DA system and brain network organization likely creates a vulnerable period in adolescence for stressors to increase risk for psychosis. The goal of this dissertation was to further our understanding of discrimination as a risk factor for psychosis by integrating psychological and neurobiological mechanisms as well as developmental processes. Study 1 investigated the psychological and behavioral mechanisms linking discrimination to subclinical psychotic-like experiences, focusing on cognitive and emotional disturbances. We found that discrimination predicts both positive and negative psychotic-like experiences, but via unique mechanisms. Study 2 sought to determine the effects of discrimination on functional brain connectivity in CHR youth. The primary finding was that discrimination did not impact connectivity patterns uniformly across adolescence and young adulthood. The relationship between reported discrimination and connectivity was moderated by age. Study 3 leveraged findings from the first two studies to improve the prediction of long-term outcomes in CHR youth, focusing on functional connectivity changes and psychological factors as mediators of discrimination's impact on outcomes. The functional connectivity patterns identified in Study 2 predicted negative symptoms and functioning outcomes. Connectivity patterns associated with risk and patterns associated with resilience were identified.