Thus, mounting evidence suggests that the key self-aggregating proteins in different proteinopathies, such as Aβ in AD, alpha-synuclein (α-syn) in PD, and prion protein (PrPc) in prion diseases share similar biophysical properties that may affect their biochemical interrelations with membrane-integrated molecular compounds (Goedert, 2015; Ugalde et al., 2016). This evidence concerns the gene PRNP and proteostasis deficiencies.