In line with our hypothesis of B/AA APOE ε4-carriers exhibiting a different plasma apoE profile compared to NHWs, potentially underlying their lower APOEε4-promoted risk of AD, we indeed found significantly higher levels of plasma apoE in B/AA APOE ε4/ε4-carriers compared to NHWs with the same genotype, despite the very small sample size. This evidence concerns the gene APOE and Alzheimer disease.