The dominant hypothesis explaining AD pathogenesis, the amyloid cascade hypothesis, proposes that changes in the level and/or activity of Aβ, in particular the accumulation of toxic small, soluble oligomers of Aβ (Aβo), trigger a cascade of events, including pathological changes in tau, that drive disease development (Hardy and Higgins, 1992). This evidence concerns the gene MAPT and Alzheimer disease.