APP and Alzheimer disease: Besides the canonical disease-associated intracellular pTau and extracellular Aβ accumulations, recent studies unraveled additional processes that could contribute to AD progression, including: (i) the intracellular accumulation of Aβ [17,18] and other APP-derived fragments [18,19,20,21,22,23,24], and (ii) the spreading of both extracellular Tau and Aβ between neurons and between neurons and glial cells [25,26].