While accumulating Aβ presents as a key initiator, but difficult disease-modifying target, there is a growing focus on multi-targeted strategies aiming at including key pathogenetic targets downstream of Aβ, which include Tau [11, 57] and its prion-like or templated propagation and neuroinflammatory changes [40, 64, 80, 99] as key pathogenetic processes in AD. Here, MAPT is linked to Alzheimer disease.