| 刘笑歌，韩冠先，郭政丽.阿尔茨海默病中细胞衰老的分子机制及中医药干预策略的研究进展[J].中医药信息,2026,43(6):77-82 |
| 阿尔茨海默病中细胞衰老的分子机制及中医药干预策略的研究进展 |
| Research Progress on the Molecular Mechanisms of Cellular Senescence in Alzheimer Disease and Intervention Strategies of Traditional Chinese Medicine |
| 投稿时间：2025-11-27 录用日期：2025-12-19 |
| DOI：10.19656/j.cnki.1002-2406.20260612 |
| 中文关键词: 阿尔茨海默病 细胞衰老 衰老相关分泌表型 分子机制 中医药干预 |
| 英文关键词: Alzheimer disease Cellular senescence Senescence－associated secretory phenotype Molecular mechanism Intervention of traditional Chinese medicine |
| 基金项目:国家中医药管理局全国名老中医专家传承工作室建设项目（第七批继承工作，No：国中医药人教函[2022]76号） |
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| 中文摘要: |
| 阿尔茨海默病（AD）是一种常见的神经退行性疾病，其发病机制复杂，目前缺乏有效的根治手段。近年来，细胞衰老作为一种稳定的细胞周期停滞状态，被证实在中枢神经系统衰老及AD病理进程中扮演关键角色。衰老细胞在AD患者大脑中大量积聚，通过分泌衰老相关分泌表型（SASP），加剧神经炎症、Aβ沉积、Tau蛋白过度磷酸化及神经元功能损伤等，从而促进疾病进展。中医药具有多成分、多靶点的特点，可通过调控细胞衰老以改善AD。本文旨在综述AD中细胞衰老的核心分子机制，以及其与AD核心病理的相互作用，并总结中医药通过调节自噬、减轻氧化应激、抑制神经炎症等途径发挥神经保护作用的机制，发现通过靶向清除衰老细胞或干预其相关通路可减轻AD病理、改善认知功能。 |
| 英文摘要: |
| Alzheimer disease （AD） is a prevalent neurodegenerative disorder characterized by a complex pathogenesis， and it remains incurable with currently available treatments. In recent years， cellular senescence， a stable state of cell cycle arrest， has been shown to play a critical role in the aging of the central nervous system and the pathological progression of AD. Senescent cells accumulate extensively in the brains of AD patients and exacerbate neuroinflammation， Aβ deposition， hyperphosphorylation of Tau protein， and neuronal dysfunction through the secretion of the senescence－associated secretory phenotype （SASP）， thereby promoting disease progression. Traditional Chinese medicine （TCM）， with its multi－component and multi－target characteristics， can improve AD by regulating cellular senescence. This study aims to summarize the core molecular mechanisms of cellular senescence in AD and its interactions with key AD pathologies. It also highlights the neuroprotective mechanisms of TCM through regulating autophagy， alleviating oxidative stress， and inhibiting neuroinflammation. Furthermore， targeting the clearance of senescent cells or intervening in related pathways may alleviate AD pathology and improve cognitive function. |
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