Han Jialin, Zhang Zhi, Zhang Pengfei, Yu Qian, Cheng Qian, Lu Zhiming, Zong Shuai
Department of Clinical Laboratory, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.
Department of Clinical Laboratory, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.
Front Neurosci. 2025 May 7;19:1575453. doi: 10.3389/fnins.2025.1575453. eCollection 2025.
Alzheimer's disease (AD) is a typical neurodegenerative disease, with the most highlighted pathologic changes identified in the -amyloid peptide (Aβ) and neurofibrillary tangles (NFTs). Aβ cascade hypothesis, which has seemed to convincingly elucidate the AD pathogenic mechanism, is becoming increasingly disproved, indicating that it is no longer able to explain the emergence of AD entirely. Neuroinflammation offers an alternative explanation for the development of AD. This paper presents an overview of the influence of microglia and astrocytes on neuroinflammation of AD. We further examine the interplay between microglia and astrocyte and their roles as inflammatory mediators. It is hypothesized that targeting these molecular mechanisms associated with neuroinflammation and controlling risk factors may provide a viable therapeutic approach for AD.
阿尔茨海默病(AD)是一种典型的神经退行性疾病,其最显著的病理变化是在β淀粉样肽(Aβ)和神经原纤维缠结(NFTs)中发现的。Aβ级联假说似乎曾令人信服地阐明了AD的致病机制,但现在越来越多地被证伪,这表明它已不再能够完全解释AD的发生。神经炎症为AD的发展提供了另一种解释。本文概述了小胶质细胞和星形胶质细胞对AD神经炎症的影响。我们进一步研究了小胶质细胞和星形胶质细胞之间的相互作用及其作为炎症介质的作用。据推测,针对这些与神经炎症相关的分子机制并控制风险因素可能为AD提供一种可行的治疗方法。