In a physiological state, AVs that are rich in Aβs are transported retrogradely to the neuronal soma where they can fuse with the lysosome and become degraded efficiently by acidified proteases [74,75,76]; however, with the progression of AD, the hyperphosphorylation of Tau impairs microtubule binding and assembly, further impedes the AV-lysosome fusion and retrograde transportation, which in turn leads to a more rapid accumulation of AVs in the dystrophic neurites [66]. Here, MAPT is linked to Alzheimer disease.