A brief historical summary of ACH, according to Herrup [18] and others [24,39] can be spotted: (1) the discovery that the core of amyloid plaques consists of a 40-amino acid protein arranged in fibrils (βA) [87]; (2) increased production or reduced clearance of βA (a fragment of APP) led to cerebral accumulation of βA; (3) multiple studies, notably those of Dennis Selkoe’s [88] using cultured cells from AD patients, suggested that βA is neurotoxic. This evidence concerns the gene APP and Alzheimer disease.