The anatomical disconnect between amyloid and tau pathologies arises, because Aβ42 aggregation and formation of plaques occurs particularly in the terminal fields of such AD vulnerable neurons, both in distal axons and dendrites, Aggregating Aβ42 eventually breaks through the cell membrane of terminals to become extracellular (Willén et al., 2017), whereupon it can act as a nidus for plaque formation recruiting also secreted extracellular Aβ. This evidence concerns the gene MAPT and amyloidosis.