APP and familial Alzheimer disease: At least two additional “facts”—the report that senile plaques are formed by Aβ deposits (Glenner and Wong, 1984) and the discovery of rare hereditary forms of early onset Familial Alzheimer’s Disease (FAD), where genetic mutations of amyloid precursor protein and presenilins lead to increased Aβ production (Levy et al., 1990; Hardy et al., 1998)—made Aβ the key factor in AD.