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Some Alzheimer's biomarkers differ by race, NIA-funded study finds

Nurse and female patient looking at a chartA new study funded by NIA points to differences in some biological markers underlying Alzheimer’s disease in African Americans and non-Hispanic whites. The results, published online Jan. 7 in JAMA Neurology, add to growing evidence of different biological mechanisms when considering race and Alzheimer’s. An accompanying editorial emphasizes that gathering biological data from African Americans is essential to furthering research in Alzheimer’s health disparities.

It’s been difficult to explain why Alzheimer’s disproportionately affects African Americans, in part because they are under-represented in studies of dementia. The new study from researchers at Washington University School of Medicine, St. Louis, looked at biomarkers, using the largest set of fluid biomarker data from African Americans to date, collected for more than a decade.

The researchers analyzed biomarker data for 1,255 participants (average age, 70), including 173 African Americans, who had enrolled in studies at the Washington University’s Knight Alzheimer’s Disease Research Center. In each racial group, 67 percent of participants had normal cognition, and the rest were mildly impaired. All had undergone at least one Alzheimer’s biomarker test, including brain scans to measure brain shrinkage and harmful forms of the amyloid protein, as well as lumbar punctures to collect cerebrospinal fluid (CSF), which reveals levels of amyloid and another protein, tau, indicating the disease processes.

Although there were no differences between African Americans and whites on some measures, including amyloid levels in the brain and CSF, other test results showed differences. Compared with whites, African Americans with a family history of dementia had a smaller hippocampus, a brain structure important for learning and memory.

Also, African Americans had significantly lower levels of tau in CSF than whites when both had the APOE ɛ4 gene form, a genetic risk factor for Alzheimer’s. Generally, lower tau—which forms damaging tangles inside neurons—means a person is less likely to be cognitively impaired, but African Americans were just as impaired as whites. It’s possible that CSF tau levels found to be abnormal in whites are not abnormal in African Americans because APOE ɛ4 exerts a weaker effect in African Americans, the authors suggested.

“The authors conclude that racial differences in AD biomarkers suggest possible race-dependent biological mechanisms that contribute to expression of disease,” wrote Lisa L. Barnes, Ph.D., of the Rush Alzheimer’s Disease Center, Chicago, in her editorial.

Future studies of Alzheimer’s biomarkers in African Americans should consider the influence of other diseases and social factors such as discrimination and education, the researchers wrote. Also, because there are relatively few lumbar puncture results from African Americans, it would be helpful to combine data from several centers and projects to generate a larger sample, Dr. Barnes suggested.

This research was funded in part by NIA grants P50AG05681, P01AG03991, and P01AG026276.

References:

Morris JC, et al. Assessment of racial disparities in biomarkers for Alzheimer’s disease. JAMA Neurology. doi:10.1001/jamaneurol.2018.4249. Published online Jan. 7, 2019.

Barnes LB. Biomarkers for Alzheimer dementia in diverse racial and ethnic minorities—a public health priority. JAMA Neurology. doi:10.1001/jamaneurol.2018.3444. Published online Jan. 7, 2019.