Accumulating evidence supports the idea that intracellular aggregates formed by tau, α-synuclein, TDP-43, SOD1, and mutant huntingtin (mHtt) transfer from cell to cell and self-replicate by recruiting natively-folded versions of the same protein, analogous to how infectious prion protein (PrPSc) templates the conformational change of soluble PrPC in prion diseases (Vaquer-Alicea and Diamond, 2019). This evidence concerns the gene PRNP and prion disease.