Additionally, the polymorphisms of the APOE gene linked to AD cases and distinct tau strains propose a imaginable parallel to circumstances noticed with human prions, where the interplay between common polymorphisms in the prion protein gene (PRNP) and variable conformational characteristics of the pathogenic prion protein leads to vastly different disease clinicopathological outcomes [47,48,64]. The gene discussed is MAPT; the disease is Alzheimer disease.