Abstract
Previous studies have consistently suggested that the varepsilon4 allele of apolipoprotein E (APOE) gene is a major risk factor for Alzheimer's disease (AD). However, whether the varepsilon2 allele, a possible protective factor for AD, will express its protective effect in terms of cortical thickness in healthy elderly carriers is unclear. The goal of this study is to clarify the effects of APOE genotypes on cortical thickness in nondemented elderly subjects. We used 164 healthy, cognitively normal, elderly subjects, who were grouped into varepsilon2 carriers, varepsilon3 homozygotes, and varepsilon4 carriers respectively. The APOE varepsilon2 carriers had a significant thicker (corrected p<0.05) cortical thickness in the superior temporal cortex compared with the varepsilon3 homozygotes. In addition to this area, the APOE varepsilon2 carriers had a significantly thicker region in the dorsolateral prefrontal cortex (corrected p<0.05) than did the varepsilon4 carriers. These findings suggest that the different alleles of the APOE gene have distinct neuroanatomic effects in elderly healthy subjects and may play specific roles in the development of AD.