In recent years, the compelling presence of insoluble, β-enriched proteinaceous aggregates lead the researchers to speculate that some of these proteins would behave like the prion protein, such as amyloid-β and Tau, the major constituent of Alzheimer’s disease (AD) plaques and tangles, α-synuclein in Parkinson’s disease and others. Here, PRNP is linked to Alzheimer disease.