Abstract

Protective variants of genetic loci are of particular interest for two reasons: first, because they are important from a clinical genetic perspective; and second, because they may give mechanistic clues about potential therapeutic strategies. In Alzheimer’s disease, the most prevalent protective allele is APOE2 (encoding apolipoprotein E2), which has a population allele frequency of approximately 10%.1 With regard to the age at onset, sporadic Alzheimer’s disease is delayed by approximately 10 years in persons with APOE2 homozygosity as compared with the general population.2-4 APOE2 heterozygosity delays the onset of sporadic Alzheimer’s disease by approximately 5 years (relative to APOE3 homozygosity) . . .

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