The most popular models are based on overexpression of human amyloid precursor protein (APP), presenilin (PSEN) [part of the γ-secretase complex involved in the cleavage of APP into amyloid-β (Aβ)] and tau, alone or in combination, to trigger accumulation of high levels of Aβ into plaques as well as the development of tauopathy (Spires and Hyman, 2005). The gene discussed is MAPT; the disease is tauopathy.