Deposition of β amyloid (Aβ) in hippocampus is a crucial progression in the pathophysiology of Alzheimer′s disease (AD). Decreasing its formation and/or increasing its clearance have become a focus of AD therapy. As compared with increased Aβ production, decreased Aβ degradation plays a more important role in AD pathogenesis. Although Aβ can be cleared through transportation to the blood and cerebral spinal fluid pathway, the so-called "vascular system", most Aβ peptide was degraded to small molecules by a kind of protease called Aβ degrading enzyme represented by neprilysin (NEP). In the olderly, mild cognitive impairment and AD patients, the NEP activity is decreased, and the decreased NEP activity is correlated with Aβ content in brain and cognitive function impairment. If NEP activity was increased to degrade Aβ, it may inhibit AD progression and even have disease-modifying potential in AD and NEP thus may behave as a potential drug target for AD therapy.