The fact that AD- and PD-associated protein particles share nucleation-dependent protein aggregation as the molecular mechanism of their origin and other properties with prions, but not the latter’s obvious infectiousness (i.e., communicability or even contagiousness), is reflected in the term “prionoid” that has been introduced to designate prion-like seeding-active forms of Aβ, tau or α-synuclein [1, 2]. This evidence concerns the gene MAPT and Alzheimer disease.