MAPT and Alzheimer disease: According to this hypothesis, a number of studies in mice have revealed that forced cell cycle re-entry in response to oncogene expression leads to the neuropathological hallmarks of AD, including Tau phosphorylation and neurofibrillary tangles [161,162], extracellular Aβ deposits [161], gliosis [163,164], synaptic dysfunction [165], neuronal death [163,165], and cognitive deficits [163], reinforcing that this process participates in the etiology of AD.