临床荟萃 ›› 2026, Vol. 41 ›› Issue (10): 948-954.doi: 10.3969/j.issn.1004-583X.2026.10.013
收稿日期:2026-09-30
出版日期:2026-10-20
发布日期:2026-10-10
通讯作者:
才延辉
E-mail:MD_CAI@163.com
基金资助:
Received:2026-09-30
Online:2026-10-20
Published:2026-10-10
摘要:
阿尔茨海默病(Alzheimer’s disease,AD)是最常见的年龄相关性神经退行性疾病,其发生发展与脑能量代谢紊乱和慢性神经炎症密切相关。AD中小胶质细胞活化伴随显著的糖代谢重编程,主要表现为糖酵解增强、氧化磷酸化受损及磷酸戊糖途径分流改变,其过程受糖酵解关键酶及mTOR-HIF-1α、腺苷酸活化蛋白激酶、TREM2-APOE等信号调控。糖代谢重编程具有明显的阶段依赖性:早期适度糖酵解增强可支持小胶质细胞迁移、吞噬和炎症应答,而慢性β-淀粉样蛋白刺激可导致糖酵解与氧化磷酸化双重障碍、氧化应激及免疫功能失调;磷酸戊糖途径来源的还原型烟酰胺腺嘌呤二核苷酸磷酸则兼具抗氧化和促进NADPH氧化酶介导活性氧生成的双重作用。本文综述AD中小胶质细胞糖代谢重编程的主要机制、功能影响及潜在干预策略,为靶向免疫代谢治疗提供参考。
中图分类号:
赵奕萌, 罗羽欣, 才延辉. 阿尔茨海默病中小胶质细胞糖代谢重编程的机制研究进展[J]. 临床荟萃, 2026, 41(10): 948-954.
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