In view of the notion that deregulation in NGF/TrkA signaling favors the amyloidogenic processing in affected neurons [39,42,44] and that tau reduction prevents the Aβ induced defects on synapses integrity and functions [123,125], these findings appear particularly relevant for tau physiopathology in the field of AD and other tauopathies, helping to develop a best-targeted and more effective tau-based immunotherapy based on the depletion of intracellular/extracellular toxic tau species [148,149]. Here, NGF is linked to Alzheimer disease.