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阿尔茨海默病（AD）作为一种临床常见的中枢神经系统退行性疾病，严重威胁着人类健康与社会发展。其发病机制与大脑中β-淀粉样蛋白（Aβ）沉积、Tau蛋白积累及过度磷酸化等密切相关。c-abl激酶能影响多条与Aβ、Tau蛋白有关的信号通路，促进神经炎症反应、响应氧化应激信号，其过度表达可导致神经元损伤，使机体出现认知及记忆能力下降等临床表现。本文围绕c-abl激酶与AD发病的关系、c-abl激酶抑制剂治疗AD的可行性及局限性等方面的研究进展进行综述，以期为AD的治疗提供新思路。

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.