期刊
NEUROLOGY
卷 96, 期 11, 页码 E1491-E1500出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1212/WNL.0000000000011599
关键词
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资金
- Alzheimer's Association [AARFD-18-562691]
- Stanford Aging and Ethnogeriatrics [SAGE 1227707-711WAKTZ, K01 AG051718]
This study found differences in amyloid PET between non-Hispanic White and Black participants who passed initial screening for the A4 study, with lower amyloid levels observed in Black participants. The effect of race on amyloid was strongest in the APOE epsilon 4 group, and within Black participants, those with lower percentage of African ancestry had higher amyloid levels.
Objective To examine whether amyloid PET in cognitively normal (CN) individuals screened for the Anti-Amyloid in Asymptomatic Alzheimer's Disease (A4) study differed across self-identified non-Hispanic White and Black (NHW and NHB) groups. Methods We examined 3,689 NHW and 144 NHB participants who passed initial screening for the A4 study and underwent amyloid PET. The effect of race on amyloid PET was examined using logistic (dichotomous groups) and linear (continuous values) regression controlling for age, sex, and number of APOE epsilon 4 and APOE epsilon 2 alleles. Associations between amyloid and genetically determined ancestry (reflecting African, South Asian, East Asian, American, and European populations) were tested within the NHB group. Potential interactions with APOE were assessed. Results NHB participants had lower rates of amyloid positivity and lower continuous amyloid levels compared to NHW participants. This race effect on amyloid was strongest in the APOE epsilon 4 group. Within NHB participants, those with a lower percentage of African ancestry had higher amyloid. A greater proportion of NHB participants did not pass initial screening compared to NHW participants, suggesting potential sources of bias related to race in the A4 PET data. Conclusion Reduced amyloid was observed in self-identified NHB participants who passed initial eligibility criteria for the A4 study. This work stresses the importance of investigating AD biomarkers in ancestrally diverse samples as well as the need for careful consideration regarding study eligibility criteria in AD prevention trials.
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