Addressing these questions in this age stratum is critical because the emergence of disparities and potential impact of modifiable factors are greatest in midlife.19 While our overall hypothesis was that, with appropriate weighting for population representativeness, there would be no differences in AD biomarker concentrations across racial and ethnic groups, we anticipated that medical and genetic (ie, APOE genotype) correlates would differ among groups, reflecting the various potential pathways that shape AD risk. This evidence concerns the gene APOE and Alzheimer disease.