细胞衰老与小胶质细胞极化在阿尔茨海默病发病机制中的研究进展

阿尔茨海默病（AD）是一种复杂的神经退行性疾病，其发病机制尚未完全阐明。近年来，细胞衰老和小胶质 细胞极化在 AD 的病理过程中发挥重要作用。细胞衰老是指细胞在经历一定的应激后进入一种不可逆的静止状 态，影响其功能，并促进神经退行性变。小胶质细胞极化状态对神经炎症及细胞微环境的改变具有重要影响。本 文综述细胞衰老、小胶质细胞极化及其在 AD 中的作用，发现两者以神经炎症这一病理环节作为链接而相互影 响，即细胞衰老影响小胶质细胞极化和功能活性，小胶质细胞的过度活化则促进衰老，如此恶性循环，从而加速 AD 进程。这些发现对 AD 治疗有潜在启示，能为 AD 的早期干预提供新思路。

Alzheimer’s disease (AD) is a complex neurodegenerative disease, its pathogenesis has not been fully elucidated. In recent years, cellular senescence and microglial polarization have played important roles in the pathological process of AD. Cellular senescence refers to irreversible state in which cells enter a quiescent state after experiencing certain stress, affecting their function, and promoting neurodegeneration. Microglial polarization state has a significant impact on neuroinflammation and changes in cellular microenvironment. This article reviews cellular senescence, microglial polarization, and their roles in AD, found that the two interact with each other through pathological link of neuroinflammation, cellular senescence affects polarization and functional activity of microglia, while excessive activation of microglia promotes senescence, such a vicious cycle, thereby accelerating AD process. These findings have potential implications in the treatment of AD, and can provide new ideas for early intervention of AD.