Tianjiu Research and Development Center for Exercise Nutrition and Foods, Hubei Key Laboratory of Exercise Training and Monitoring, College of Sports Medicine, Wuhan Sports University, Wuhan, 430079, China.
J Neuroinflammation. 2023 Mar 19;20(1):76. doi: 10.1186/s12974-023-02753-6.
Alzheimer's disease (AD) is a chronic neurodegenerative disease, with the characteristics of neurofibrillary tangle (NFT) and senile plaque (SP) formation. Although great progresses have been made in clinical trials based on relevant hypotheses, these studies are also accompanied by the emergence of toxic and side effects, and it is an urgent task to explore the underlying mechanisms for the benefits to prevent and treat AD. Herein, based on animal experiments and a few clinical trials, neuroinflammation in AD is characterized by long-term activation of pro-inflammatory microglia and the NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasomes. Damaged signals from the periphery and within the brain continuously activate microglia, thus resulting in a constant source of inflammatory responses. The long-term chronic inflammatory response also exacerbates endoplasmic reticulum oxidative stress in microglia, which triggers microglia-dependent immune responses, ultimately leading to the occurrence and deterioration of AD. In this review, we systematically summarized and sorted out that exercise ameliorates AD by directly and indirectly regulating immune response of the central nervous system and promoting hippocampal neurogenesis to provide a new direction for exploring the neuroinflammation activity in AD.
阿尔茨海默病(AD)是一种慢性神经退行性疾病,其特征是神经纤维缠结(NFT)和老年斑(SP)的形成。尽管基于相关假说的临床试验已经取得了很大进展,但这些研究也伴随着毒性和副作用的出现,探索潜在机制以预防和治疗 AD 是当务之急。在此,基于动物实验和一些临床试验,AD 中的神经炎症表现为小胶质细胞的长期过度激活和 NOD、LRR 和 pyrin 结构域包含蛋白 3(NLRP3)炎性小体。来自外周和大脑内部的受损信号持续激活小胶质细胞,从而导致炎症反应的持续来源。长期的慢性炎症反应也加剧了小胶质细胞内质网氧化应激,引发小胶质细胞依赖性免疫反应,最终导致 AD 的发生和恶化。在这篇综述中,我们系统地总结和整理了运动通过直接和间接调节中枢神经系统的免疫反应和促进海马神经发生来改善 AD,为探索 AD 中的神经炎症活动提供了新的方向。