APOE and prion disease: However, the limited number of clinical cases and well-recognized complexity of human prion disease, which includes factors like codon 129 polymorphism, PrPSc subtypes, and variable presence of Aβ co-pathology [33, 79], render systematic analysis of the APOE polymorphism effect on disease progression in human prion entities arduous to conduct and inherently underpowered [126].