Longitudinal Biological Pathways Leading to Alzheimer's Disease Health Disparities in Blacks
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PROJECT SUMMARY Blacks are more than twice as likely to develop dementia than Whites. However, controlling for many of the factors that put Blacks at greater risk, such as having less education and lower occupational status, does not eliminate these health disparities. Therefore, other race-related factors underlie the increased risk for dementia, including Alzheimer's disease (AD). One possibility is that multiple levels of chronic stress found uniquely in Blacks, exacerbate these health disparities. As outlined by the NIA's Health Disparities Research Framework, these stressors stem from environmental factors such as residential segregation, sociocultural factors such as racism, and behavioral factors such as one's perceived control. It is clear that these types of stressors negatively impact mental health, but a large gap exists between a) these generalized stressors, b) neurobiological pathways, and c) a diagnosis of AD in Blacks. Because AD is a brain disease, this knowledge gap can be illuminated by understanding the biological progression from “normal” to AD in Blacks. According to the neurotoxicity hypothesis, prolonged exposure to stress increases the brain's vulnerability to pathological toxins and reduces the brain's ability to resist subtle brain damage. Thus, unique race-related stressors might lead to a brain environment that is more vulnerable to AD pathology (beta-amyloid and tau) and accelerates declines in brain structure and the associated cognitive declines that lead to AD in Blacks compared with Whites. By harmonizing data from the National Alzheimer's Coordinating Center and the Minority Aging Research Study, secondary analyses will be conducted to analyze the biological pathways that create and sustain race-related health disparities in AD. We will use multi-level model regression techniques to test the extent that 1) rates of longitudinal declines in cortical thickness will be associated with greater cognitive decline in Blacks than Whites and 2) rates of longitudinal declines in hippocampal volumes and a novel measure of hippocampal complexity will be associated with greater cognitive decline in Blacks than Whites. Addressing whether Blacks are more vulnerable to longitudinal cognitive decline through different neurodegenerative pathways than Whites would lead to a theoretical framework that would provide testable hypotheses of causes of these potential vulnerabilities (like racial stressors).
