Alzheimer disease （AD） is a progressive neurodegenerative disease characterized by a decline in learning and memory， impairment of multiple cognitive domains， and ultimately inability to perform daily tasks. More and more evidence suggests that targeting Aβ production to reduce its deposition is a therapeutic option for AD pathology. As a key secretory enzyme in the process of amyloid precursor protein cleavage， ADAM10 can not only reduce the production of Aβ， but also affect the pathology of AD， including reducing tau protein hyperphosphorylation， maintaining normal synaptic function， and promoting hippocampal neurogenesis and neuronal network homeostasis. ADAM10 may be a biomarker for early and accurate diagnosis of AD. This article will review the nature of ADAM10 and its role in the pathogenesis of AD， and discuss the potential of ADAM10 as a target for the treatment of AD， in order to provide a theoretical basis and new ideas for the in-depth study and treatment of AD.