As individuals age, gradual changes in memory, learning and decision-making naturally occur; however, accelerated rates of cognitive decline may be signs of impending impairment and dementia. Racial and ethnic minorities carry a greater dementia burden than whites with a prevalence and incidence rate approximately 2-3 times higher among blacks than whites. These disparities are often attributed to differences in socioeconomic status, lifestyle factors, chronic conditions and childhood conditions. While accounting for these factors tends to reduce these disparities, the black-white difference often persists, warranting examination of other determinants of this inequity, particularly at earlier stages of the life course. Recent research suggest that cognitive decline among blacks begins during mid-life. This earlier rate of decline may be due to differential exposure to mid-life acute and chronic stressors. Older racial and ethnic minorities generally report greater exposure to stress compared to whites, which puts them at greater risk for poor health. These stressors can accelerate dysregulation of key physiological systems, including the cardiovascular, metabolic and immune systems, which are associated with cognitive outcomes. Thus, race differences in stress exposure that lead to differences in physiological functioning may be one pathway through which stressors differentially affect the cognitive function of blacks and whites. Additionally, social resources, such as social support, engagement and integration are associated with positive cognitive outcomes and may protect against the negative effects of acute and chronic stressors on change in cognitive function. The overarching goal of this proposal is to assess the role of acute and chronic stressors, social resources and physiological dysregulation on black-white differences in change in cognitive function. We will: determine whether acute and chronic stressors during mid- life are associated with cognitive decline and whether they explain black-white differences in cognitive decline (Aim 1); examine whether change in physiological dysregulation mediates the relationship between mid-life stress and cognitive decline (Aim 2); and, determine whether mid-life availability of social resources influences the relationship between stress and cognitive decline (Aim 3). Finally, we will test a conceptual model for cognitive decline that incorporates acute and chronic stressors, social resources and physiological dysregulation across race- and sex-specific groups (Aim 4). To achieve these aims, we will use data from the Health and Retirement Study and linear mixed effects models that include random intercepts and random slopes. The findings from this research will improve our understanding of mid-life factors that influence aging and disparities in cognitive function, thus aligning with Goal B and F of the National Institute on Aging?s Strategic Plan. This research will also help identify points of intervention and modifiable risk and protective factors for cognitive decline, which aligns with the objectives of PA-18-850.
The burden of dementia disproportionately affects blacks with a prevalence 2-3 times higher than whites. This disparity may be due to earlier declines in cognitive function among blacks, their disproportionate exposure to stressors and limited access to protective resources during mid-life. To improve our understanding of racial disparities in cognitive function and inform dementia prevention efforts, this project investigates the roles of mid-life acute and chronic stressors, social resources, and physiological dysregulation on black-white difference in cognitive decline.
