期刊
ANNALS OF NEUROLOGY
卷 89, 期 2, 页码 254-265出版社
WILEY
DOI: 10.1002/ana.25948
关键词
-
资金
- National Institute of Health (NIH) [R01NR012907, R01NR012657, R01NR014449, P01AG00391, P01AG026276, P01AG005681]
- Barnes-Jewish Hospital
- Washington University Institute of Clinical and Translational Sciences Foundation [UL1 TR000448]
- Hope Center for Neurological Disorders
- Paula and Rodger O. Riney Fund
- Daniel J. Brennan MD Fund
- Fred Simmons and Olga Mohan Fund
- Avid Radiopharmaceuticals [18F-AV-45, 18F-AV-1451]
This study examined racial differences in neuroimaging biomarkers for Alzheimer's disease dementia between African American and white participants, finding that African Americans showed greater neurodegeneration. Socioeconomic status was found to mediate the relationship between race and neuroimaging measures, highlighting the importance of social and environmental factors in contributing to racial disparities in Alzheimer's disease.
Objectives African Americans are at greater risk for developing Alzheimer's disease (AD) dementia than non-Hispanic whites. In addition to biological considerations (eg, genetic influences and comorbid disorders), social and environmental factors may increase the risk of AD dementia. This paper (1) assesses neuroimaging biomarkers of amyloid (A), tau (T), and neurodegeneration (N) for potential racial differences and (2) considers mediating effects of socioeconomic status (SES) and measures of small vessel and cardiovascular disease on observed race differences. Methods Imaging measures of AT(N) (amyloid and tau positron emission tomography [PET]) structural magnetic resonance imaging (MRI), and resting state functional connectivity (rs-fc) were collected from African American (n = 131) and white (n = 685) cognitively normal participants age 45 years and older. Measures of small vessel and cardiovascular disease (white matter hyperintensities [WMHs] on MRI, blood pressure, and body mass index [BMI]) and area-based SES were included in mediation analyses. Results Compared to white participants, African American participants had greater neurodegeneration, as measured by decreased cortical volumes (Cohen's f(2) = 0.05, p < 0.001). SES mediated the relationship between race and cortical volumes. There were no significant race effects for amyloid, tau, or rs-fc signature. Interpretation Modifiable factors, such as differences in social contexts and resources, particularly area-level SES, may contribute to observed racial differences in AD. Future studies should emphasize collection of relevant psychosocial factors in addition to the development of intentional diversity and inclusion efforts to improve the racial/ethnic and socioeconomic representativeness of AD studies. ANN NEUROL 2020
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