Objective:To test the hypothesis that neighborhood-level disadvantage is associated with longitudinal measures of neurodegeneration and cognitive decline in an unimpaired cohort.Methods:Longitudinal MRI and cognitive testing data were collected from 601 cognitively unimpaired participants in the Wisconsin Registry for Alzheimer’s Prevention study and the Wisconsin Alzheimer’s Disease Research Center clinical cohort. Area Deprivation Index was geospatially determined based on participant residence geocode and ranked relative to state of residence. Linear regression models were fitted to test associations between neighborhood-level disadvantage and longitudinal change in cortical thickness and cognitive test performance. Mediation tests were used to assess whether neurodegeneration and cognitive decline were associated with neighborhood-level disadvantage along the same theoretical causal path.Results:In our middle to older aged study population (mean baseline age=59), living in the 20% most disadvantaged neighborhoods (N=19) relative to state of residence was associated with cortical thinning in Alzheimer’s signature regions (p=0.002) and decline in the Preclinical Alzheimer’s disease Cognitive Composite (p=0.04), particularly the Trails-Making Test Part B (p<0.001), but not Rey Auditory Verbal Learning Test (p=0.77) or Story Memory Delayed Recall (p=0.49) subtests. Associations were attenuated but remained significant after controlling for racial and demographic differences between neighborhood-level disadvantage groups. Cortical thinning partially mediated the association between neighborhood-level disadvantage and cognitive decline.Conclusions:In this longitudinal study of cognitively unimpaired adults, living in the most highly disadvantaged neighborhoods was associated with accelerated degeneration in Alzheimer’s signature regions and cognitive decline. This study provides further evidence for neighborhood-level disadvantage as a risk factor for preclinical neurodegeneration and cognitive decline in certain populations. Limitations of the present study, including a small number of participants from highly disadvantaged neighborhoods and a circumscribed geographic setting, should be explored in larger and more diverse study cohorts.
Black Americans are disproportionately affected by dementia. To expand our understanding of mechanisms of this disparity, we look to Alzheimer's disease (AD) biomarkers. In this review, we summarize current data, comparing the few studies presenting these findings. Further, we contextualize the data using two influential frameworks: the National Institute on Aging–Alzheimer's Association (NIA‐AA) Research Framework and NIA's Health Disparities Research Framework. The NIA‐AA Research Framework provides a biological definition of AD that can be measured in vivo. However, current cut‐points for determining pathological versus non‐pathological status were developed using predominantly White cohorts—a serious limitation. The NIA's Health Disparities Research Framework is used to contextualize findings from studies identifying racial differences in biomarker levels, because studying biomakers in isolation cannot explain or reduce inequities. We offer recommendations to expand study beyond initial reports of racial differences. Specifically, life course experiences associated with racialization and commonly used study enrollment practices may better account for observations than exclusively biological explanations.
Background: Despite many studies reporting disparities in coronavirus disease-2019 (COVID-19) incidence and outcomes in Black and Hispanic/Latino populations, mechanisms are not fully understood to inform mitigation strategies.Objective: The aim was to test whether neighborhood factors beyond individual patient-level factors are associated with in-hospital mortality from COVID-19. We hypothesized that the Area Deprivation Index (ADI), a neighborhood census-block-level composite measure, was associated with COVID-19 mortality independently of race, ethnicity, and other patient factors.
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