APOE4 homozygote females are resistant to the beneficial effects of 17β-estradiol on memory and CA1 dendritic spine density in the EFAD mouse model of Alzheimer's disease.

ABSTRACT: Female APOE4 carriers are at greatest risk of Alzheimer's disease (AD). The potent estrogen 17β-estradiol (E₂) may mediate AD risk, as the onset of memory decline coincides with the menopausal transition. Whether APOE genotype mediates E₂'s effects on memory and neuronal morphology is poorly understood. We used the APOE^+/+/5xFAD^+/- (EFAD) mouse model to examine how APOE3 homozygote (E3FAD), APOE3/4 heterozygote (E3/4FAD), and APOE4 homozygote (E4FAD) genotypes modulate effects of E₂ on object and spatial memory consolidation, dendritic spine density, and dorsal hippocampal estrogen receptor expression in 6-month-old ovariectomized EFAD mice. Dorsal hippocampal E₂ infusion enhanced memory consolidation and increased CA1 apica

SUBMITTER: Taxier LR 

PROVIDER: S-EPMC10756028 | biostudies-literature | 2022 Oct

REPOSITORIES: biostudies-literature