Numerous findings indicate that pathologically aggregated species of amyloid-β (Aβ) and tau protein in Alzheimer’s disease (AD), and of α-synuclein (αSyn) in Parkinson’s disease (PD) can act as proteinaceous nuclei (‘seeds’) which recruit endogenous precursor proteins and convert them into their own misfolded oligomeric or polymeric aggregate structures. This evidence concerns the gene YWHAQ and Alzheimer disease.