PRNP and Alzheimer disease: Again, it is the N-terminal part of PrPC that acts as the crucial docking hub for β-sheet-rich oligomeric amyloid-β (Aβ) peptides and hyperphosphorylated tau (pTau) in AD or α-synuclein in PD, thus allowing for high-affinity binding and subsequent neurotoxic signaling via additional PrPC interacting transmembrane proteins (Fig. 1) [9, 36–45].