Senescent microglia: The hidden culprits accelerating Alzheimer’s disease

IF 2.6 4区医学 Q3 NEUROSCIENCES Brain Research Pub Date : 2025-01-28 DOI:10.1016/j.brainres.2025.149480

Wu Li , Xie Yong-Yan , Mu Jia-Xin , Ge Shu-Chao , Huang Li-Ping

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Abstract

Ageing is a major risk factor for neurodegenerative diseases like Alzheimer’s disease (AD). Microglia, as the principal innate immune cells within the brain, exert homeostatic and active immunological defense functions throughout human lifespan. The age-related dysfunction of microglia is currently recognized as a pivotal trigger for brain diseases associated with aging. In AD, microglia exhibit alterations in gene expression, cellular morphology, and functional behavior. By focusing on the immunomodulatory functions of factors secreted by senescent microglia, such as cytokines, chemokines, complement factors, and reactive oxygen species (ROS), we explore the diverse detrimental effects of microglia in aging and AD pathogenesis, including Aβ accumulation, Tau deposition, synaptic dysfunction, and neuroinflammation. These collectively contribute to hastening the progression of. In this review, we highlight the key role of senescent microglia in the pathological processes of AD. Then we propose that targeting senescent microglia holds great promise for therapeutic interventions in neurodegenerative diseases.

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衰老的小胶质细胞：加速阿尔茨海默病的隐藏罪魁祸首。

衰老是阿尔茨海默病（AD）等神经退行性疾病的主要风险因素。小胶质细胞作为大脑内主要的先天免疫细胞，在人的一生中发挥着稳态和主动的免疫防御功能。与年龄相关的小胶质细胞功能障碍目前被认为是与衰老相关的脑疾病的关键触发因素。在阿尔茨海默病中，小胶质细胞表现出基因表达、细胞形态和功能行为的改变。通过关注衰老小胶质细胞分泌的因子，如细胞因子、趋化因子、补体因子和活性氧（ROS）的免疫调节功能，我们探讨了小胶质细胞在衰老和AD发病中的各种有害作用，包括Aβ积累、Tau沉积、突触功能障碍和神经炎症。这些共同有助于加速……的进展。在这篇综述中，我们强调衰老小胶质细胞在阿尔茨海默病病理过程中的关键作用。然后我们提出针对衰老小胶质细胞的治疗干预在神经退行性疾病中具有很大的前景。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Brain Research 医学-神经科学

CiteScore

5.90

自引率

3.40%

发文量

268

审稿时长

47 days

期刊介绍： An international multidisciplinary journal devoted to fundamental research in the brain sciences. Brain Research publishes papers reporting interdisciplinary investigations of nervous system structure and function that are of general interest to the international community of neuroscientists. As is evident from the journals name, its scope is broad, ranging from cellular and molecular studies through systems neuroscience, cognition and disease. Invited reviews are also published; suggestions for and inquiries about potential reviews are welcomed. With the appearance of the final issue of the 2011 subscription, Vol. 67/1-2 (24 June 2011), Brain Research Reviews has ceased publication as a distinct journal separate from Brain Research. Review articles accepted for Brain Research are now published in that journal.