APOE2 mitigates disease-related phenotypes in an isogenic hiPSC-based model of Alzheimer's disease.

ABSTRACT: Genome-wide association studies (GWAS) have identified polymorphism in the Apolipoprotein E gene (APOE) to be the most prominent risk factor for Alzheimer's disease (AD). Compared to individuals homozygous for the APOE3 variant, individuals with the APOE4 variant have a significantly elevated risk of AD. On the other hand, longitudinal studies have shown that the presence of the APOE2 variant reduces the lifetime risk of developing AD by 40 percent. While there has been significant research that has identified the risk-inducing effects of APOE4, the underlying mechanisms by which APOE2 influences AD onset and progression have not been extensively explored. In this study, we utilize an isogenic human induced pluripotent stem cell (hiPSC)-based system to demonstrate that conversion of APOE3

SUBMITTER: Brookhouser N 

PROVIDER: S-EPMC8501163 | biostudies-literature | 2021 Oct

REPOSITORIES: biostudies-literature