In fact, it is clear that if Aβ deposition occurs in response to cerebral hypometabolism in even young transgenic animals [132], and in elderly AD individuals [144,145], a search for factors that trigger pathological processes in murine and human brains, which in turn lead to APP overexpression and Aβ accumulation, is of crucial importance in current biomedical research. The gene discussed is APP; the disease is Alzheimer disease.