It has been demonstrated that the level and activity of NEP was significantly reduced in the cortex and hippocampus of AD brain, and irregular function of NEP causes a two-fold increase in the endogenous toxic Aβ40-42 levels within the brain, which lead to impaired synaptic plasticity and cognitive abnormalities that ultimately increase the risk of AD (Iwata et al.,2005; Jha et al., 2015). The gene discussed is MME; the disease is Alzheimer disease.