Luo et al. [26] proposed that the amyloid cascade hypothesis in Alzheimer’s disease should be expanded to include cross-interactions between Aβ and other amyloid proteins, like tau, human prion protein (PrPC), α-synuclein, and other proteins present in the cerebrospinal fluid during various disease conditions, such as lysozyme, transthyretin, apolipoprotein A1, and blood proteins like serum amyloid P component and fibrinogen. Here, PRNP is linked to early-onset autosomal dominant Alzheimer disease.