Even the disease-defining biochemical findings of pathology in AD, represented by Amyloid-beta (Aβ40 and Aβ42, hereafter Abeta) and phosphorylation of Tau protein (TAU for tubulin-associated unit or by the Greek letter τ, hereafter Tau; for a review, see Bloom, 2014), remain controversial as causative of disease trajectory and cognitive symptoms. This evidence concerns the gene APP and Alzheimer disease.