阿尔茨海默病的进化:从线粒体到小胶质细胞。

IF 12.4 1区 医学 Q1 CELL BIOLOGY
Feng-ge Yang , Yu-lin Liang , Xu Wang , Jun-ting Wang , Wei Gao , Qiu-yan Ye , Xue-yuan Li , Yu Yang , Hong-lin Li
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引用次数: 0

摘要

阿尔茨海默病(AD)是世界上最普遍的神经退行性疾病。最近的研究表明,线粒体功能障碍驱动小胶质细胞功能的改变,是AD发病和进展的关键机制。越来越多的证据表明,线粒体功能障碍包括能量代谢缺陷、氧化应激升高、线粒体动力学受损、自噬破坏和钙稳态失衡。这些损伤调节了小胶质细胞的激活状态,加剧了神经炎症,改变了吞噬能力,增加了细胞凋亡,共同导致了小胶质细胞功能障碍。本文就线粒体功能障碍与AD的关系作一综述,阐明线粒体功能障碍对小胶质细胞的影响。总结了针对线粒体调节小胶质细胞功能的治疗策略,旨在预防和治疗AD。目的是为阿尔茨海默病的研究和治疗提供新的视角和见解,有助于改善患者的生活质量和预后。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The evolution of Alzheimer’s disease: From mitochondria to microglia
Alzheimer’s disease (AD) represents the most prevalent neurodegenerative disorder worldwide. Recent studies highlights that mitochondrial dysfunction drives alterations in microglial function, serving as a pivotal mechanism in the pathogenesis and progression of AD. Increasingly, there is evidence that mitochondrial dysfunction encompasses energy metabolism deficits, heightened oxidative stress, impaired mitochondrial dynamics, disrupted autophagy, and calcium homeostasis imbalances. These impairments modulate microglial activation states, precipitating exacerbated neuroinflammation, altered phagocytic capacity, and increased cellular apoptosis, collectively contributing to microglial dysfunction. This paper presents a narrative review on the relationship between mitochondrial dysfunction and AD, elucidating the impact of mitochondrial impairment on microglia. It summarizes therapeutic strategies that target mitochondria to modulate microglial function, aiming to prevent and treat AD. The goal is to provide new perspectives and insights for AD research and treatment, contributing to improving patients' quality of life and prognosis.
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来源期刊
Ageing Research Reviews
Ageing Research Reviews 医学-老年医学
CiteScore
19.80
自引率
2.30%
发文量
216
审稿时长
55 days
期刊介绍: With the rise in average human life expectancy, the impact of ageing and age-related diseases on our society has become increasingly significant. Ageing research is now a focal point for numerous laboratories, encompassing leaders in genetics, molecular and cellular biology, biochemistry, and behavior. Ageing Research Reviews (ARR) serves as a cornerstone in this field, addressing emerging trends. ARR aims to fill a substantial gap by providing critical reviews and viewpoints on evolving discoveries concerning the mechanisms of ageing and age-related diseases. The rapid progress in understanding the mechanisms controlling cellular proliferation, differentiation, and survival is unveiling new insights into the regulation of ageing. From telomerase to stem cells, and from energy to oxyradical metabolism, we are witnessing an exciting era in the multidisciplinary field of ageing research. The journal explores the cellular and molecular foundations of interventions that extend lifespan, such as caloric restriction. It identifies the underpinnings of manipulations that extend lifespan, shedding light on novel approaches for preventing age-related diseases. ARR publishes articles on focused topics selected from the expansive field of ageing research, with a particular emphasis on the cellular and molecular mechanisms of the aging process. This includes age-related diseases like cancer, cardiovascular disease, diabetes, and neurodegenerative disorders. The journal also covers applications of basic ageing research to lifespan extension and disease prevention, offering a comprehensive platform for advancing our understanding of this critical field.
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