Laboratory of Exercise and Neurobiology, School of Physical Education and Sports Science, South China Normal University, Guangzhou, 510006, China.
Laboratory of Exercise and Neurobiology, School of Physical Education and Sports Science, South China Normal University, Guangzhou, 510006, China.
Biochem Biophys Res Commun. 2024 Nov 5;732:150418. doi: 10.1016/j.bbrc.2024.150418. Epub 2024 Jul 17.
Alzheimer's disease (AD) is a prevalent and debilitating brain disorder that worsens progressively with age, characterized by cognitive decline and memory impairment. The accumulation of amyloid-beta (Aβ) leading to amyloid plaques and hyperphosphorylation of Tau, resulting in intracellular neurofibrillary tangles (NFTs), are primary pathological features of AD. Despite significant research investment and effort, therapies targeting Aβ and NFTs have proven limited in efficacy for treating or slowing AD progression. Consequently, there is a growing interest in non-invasive therapeutic strategies for AD prevention. Exercise, a low-cost and non-invasive intervention, has demonstrated promising neuroprotective potential in AD prevention. Astrocytes, among the most abundant glial cells in the brain, play essential roles in various physiological processes and are implicated in AD initiation and progression. Exercise delays pathological progression and mitigates cognitive dysfunction in AD by modulating astrocyte morphological and phenotypic changes and fostering crosstalk with other glial cells. This review aims to consolidate the current understanding of how exercise influences astrocyte dynamics in AD, with a focus on elucidating the molecular and cellular mechanisms underlying astrocyte remodeling. The review begins with an overview of the neuropathological changes observed in AD, followed by an examination of astrocyte dysfunction as a feature of the disease. Lastly, the review explores the potential therapeutic implications of exercise-induced astrocyte remodeling in the context of AD.
阿尔茨海默病（AD）是一种普遍且使人虚弱的脑部疾病，会随着年龄的增长而逐渐恶化，其特征是认知能力下降和记忆力减退。β淀粉样蛋白（Aβ）的积累导致淀粉样斑块和 Tau 的过度磷酸化，从而导致细胞内神经原纤维缠结（NFTs），是 AD 的主要病理特征。尽管投入了大量的研究和努力，但针对 Aβ和 NFT 的治疗方法在治疗或减缓 AD 进展方面的疗效有限。因此，人们对 AD 预防的非侵入性治疗策略越来越感兴趣。运动是一种低成本、非侵入性的干预措施，在预防 AD 方面显示出了有希望的神经保护潜力。星形胶质细胞是大脑中最丰富的神经胶质细胞之一，在各种生理过程中发挥着重要作用，并与 AD 的起始和进展有关。运动通过调节星形胶质细胞的形态和表型变化以及促进与其他神经胶质细胞的串扰，延缓 AD 的病理进展并减轻认知功能障碍。本综述旨在综合当前对运动如何影响 AD 中星形胶质细胞动力学的理解，重点阐明星形胶质细胞重塑的分子和细胞机制。综述首先概述了 AD 中观察到的神经病理学变化，然后检查了星形胶质细胞功能障碍作为疾病的一个特征。最后，综述探讨了运动诱导的星形胶质细胞重塑在 AD 背景下的潜在治疗意义。
