The ability of protein particles, deriving from misfolding and aggregation of amyloid-β (Aβ), tau, α-synuclein (α-syn), superoxide dismutase 1 (SOD1), to transfer from one cell to another, similar to misfolded PrP, accounts for the widespread pathophysiology seen in neurodegenerative disorders such as Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS) and Huntington’s (HD) disease [10]. This evidence concerns the gene MAPT and Alzheimer disease.