Alzheimer's disease (AD) is a neurodegenerative disease of the central nervous system, seriously threatening the health and development of human beings. AD pathogenesis is related to amyloid β-protein accumulation, microtubule-associated protein Tau accumulation and hyperphosphorylation in the brain. C-abl kinase can affect signal pathways related to Aβ and Tau proteins, promote neuroinflammatory response and respond to oxidative stress signals; and its overexpression can lead to neuronal damage, resulting in clinical manifestations such as cognitive and memory decline. This paper reviews the relationship between c-abl kinase and AD pathogenesis, and feasibility and limitations of c-abl kinase inhibitors in AD, in order to provide new ideas for AD treatment.