Zhang Shenghao, Gao Zhejianyi, Feng Lina, Li Mingquan
Department of Neurology, The Third Affiliated Hospital of Changchun University of Chinese Medicine, Changchun, Jilin Province, 130021, People's Republic of China.
Department of Orthopaedics, Fushun Hospital of Chinese Medicine, Fushun, Liaoning Province, 113008, People's Republic of China.
J Inflamm Res. 2024 Oct 13;17:7235-7259. doi: 10.2147/JIR.S483412. eCollection 2024.
Alzheimer's disease (AD) is a fatal neurodegenerative disease characterized by its insidious onset and progressive development, making it the most common form of dementia. Despite its prevalence, the exact causes and mechanisms responsible for AD remain unclear. Recent studies have highlighted that inflammation in the central nervous system (CNS) plays a crucial role in both the initiation and progression of AD. Neuroinflammation, an immune response within the CNS triggered by glial cells in response to various stimuli, such as nerve injury, infection, toxins, or autoimmune reactions, has emerged as a significant factor alongside amyloid deposition and neurofibrillary tangles (NFTs) commonly associated with AD. This article aims to provide an overview of the most recent research regarding the involvement of neuroinflammation in AD, with a particular focus on elucidating the specific mechanisms involving microglia and astrocytes. By exploring these intricate processes, a new theoretical framework can be established to further probe the impact of neuroinflammation on the development and progression of AD. Through a deeper understanding of these underlying mechanisms, potential targets for therapeutic interventions and novel treatment strategies can be identified in the ongoing battle against AD.
阿尔茨海默病(AD)是一种致命的神经退行性疾病,其特点是起病隐匿、病情逐渐发展,是最常见的痴呆形式。尽管其发病率很高,但AD的确切病因和发病机制仍不清楚。最近的研究强调,中枢神经系统(CNS)的炎症在AD的发生和发展中起着关键作用。神经炎症是中枢神经系统内由胶质细胞对各种刺激(如神经损伤、感染、毒素或自身免疫反应)产生的免疫反应,已成为与AD常见的淀粉样蛋白沉积和神经原纤维缠结(NFTs)并列的一个重要因素。本文旨在概述关于神经炎症在AD中作用的最新研究,特别关注阐明涉及小胶质细胞和星形胶质细胞的具体机制。通过探索这些复杂的过程,可以建立一个新的理论框架,以进一步探究神经炎症对AD发生和发展的影响。通过更深入地了解这些潜在机制,可以在对抗AD的持续斗争中确定治疗干预的潜在靶点和新的治疗策略。