These pathogenic molecular mechanisms: (i) may be augmented by other neurotoxic pathological factors that alter polypeptide conformation and promote protein misfolding; (ii) are extraordinarily similar to those involving the generation, propagation, diffusion, and spreading of prions; and (iii) have implications for the potential “seeding” and horizontal transmission of the entire spectrum of human misfolded tau-, α-synuclein- and amyloid-beta (Aβ) peptide-linked diseases that include AD, PSP and PD (Jaunmuktane and Brandner, 2020; Carlson and Prusiner, 2021; Thomzig et al., 2021). This evidence concerns the gene MAPT and Alzheimer disease.