Because the model reproduces major features of sporadic AD (i.e., tau hyperphosphorylation, Aβ generation, and glutamate excitotoxicity), our study could provide a rationale for the documented efficacy of centrally active ACE inhibitors in several clinical studies, which showed retardation of AD-related cognitive decline as a major sign of neurodegeneration [21–25]. The gene discussed is MAPT; the disease is Alzheimer disease.