Culture, Ethnicity, and Level of Education in Alzheimer’s Disease

Alzheimer’s disease (AD) is the most frequent cause of dementia, where the abnormal accumulation of beta-amyloid (Aβ) and tau lead to neurodegeneration as well as loss of cognitive, behavioral, and functional abilities. The present review analyzes AD from a cross-cultural neuropsychological perspective, looking at differences in culture-associated variables, neuropsychological test performance and biomarkers across ethnic and racial groups. Studies have found significant effects of culture, preferred language, country of origin, race, and ethnicity on cognitive test performance, although the definition of those grouping terms varies across studies. Together, with the substantial underrepresentation of minority groups in research, the inconsistent classification might conduce to an inaccuratte diagnosis that often results from biases in testing procedures that favor the group to which test developers belong. These biases persist even after adjusting for variables related to disadvantageous societal conditions, such as low level of education, unfavorable socioeconomic status, health care access, or psychological stressors. All too frequently, educational level is confounded with culture. Minorities often have lower educational attainment and lower quality of education, causing differences in test results that are then attributed to culture. Higher levels of education are also associated with increased cognitive reserve, a protective factor against cognitive decline in the presence of neurodegeneration. Biomarker research suggests there might be significant differences in specific biomarker profiles for each ethnicity/race in need of accurate cultural definitions to adequately predict risk and disease progression across ethnic/racial groups. Overall, this review highlights the need for diversity in all domains of AD research that lack inclusion and the collection of relevant information from these groups. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s13311-022-01193-z.