Forced cell cycle re-entry in neurons results in classical hallmarks of AD, including tau protein hyperphosphorylation and neurofibrillary tangles (NFT), increased APP processing and extracellular deposits of Aβ, neuronal cell death, gliosis, and cognitive deficits [69–72], and it has been shown to enhance the phenotype of a murine model of AD [73]. This evidence concerns the gene APP and Alzheimer disease.