MAPT and Alzheimer disease: In the context of the neuroimmunomodulation hypothesis [9,10,11,12,13], we proposed that the onset of AD is mainly a consequence of the response of microglial cells to “damage signals” or tau oligomers (Figure 1), which trigger a neuro-inflammatory response, promoting an anomalous cascade of signaling that involves the release of the nuclear factor κB (NFκB), overproduction of pathological levels of cytokines and chemokines, and the consequent activation of neuronal receptors.