Long Campbell, Fritts Arianne, Broadway Jessica, Brawman-Mintzer Olga, Mintzer Jacobo
Ralph H. Johnson VA Health Care System, 109 Bee St, Charleston, SC 29401, USA.
College of Health Professions, Department of Health Sciences and Research, Medical University of South Carolina, 171 Ashley Avenue, Charleston, SC 29425, USA.
J Clin Med. 2025 Jan 8;14(2):331. doi: 10.3390/jcm14020331.
: The goal of this commentary is to highlight several key components of the inflammatory process as it relates to amyloid toxicity in Alzheimer's disease (AD), including the role of neuroinflammatory factors and peripheral inflammatory events. : Google Scholar and PubMed were used to find articles with the following keywords: Alzheimer's disease, amyloids, neuroinflammation, peripheral inflammation, microglia, cytokines, and treatments. Sources that were case reports, not peer-reviewed, or older than 30 years were excluded. Abstracts were reviewed first for their relevance before the full text was considered. Methods sections were reviewed to ensure the interventional papers included were randomized controlled trials, meta-analyses, or systematic reviews; however, several literature reviews were also included due to the relevance of their background information. : Based on the literature review, we chose to concentrate on microglia, cytokine signaling, and peripheral inflammation markers. We found that microglia activation and subsequent microglia-driven inflammation play a pivotal role in the pathomechanism of AD. Additionally, cytokines such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-a) appear to contribute to amyloid accumulation and cell damage. Finally, the increased permeability of the blood-brain barrier (BBB) allows for the peripheral inflammatory process to contribute to the inflammation of the central nervous system (CNS) and amyloid-beta (Aβ) accumulation. : Current evidence suggests that the immune system plays a pivotal role in the pathogenesis of AD, both in the CNS and the periphery.
本述评的目的是强调炎症过程的几个关键组成部分，因为它与阿尔茨海默病（AD）中的淀粉样蛋白毒性相关，包括神经炎症因子和外周炎症事件的作用。使用谷歌学术和PubMed搜索包含以下关键词的文章：阿尔茨海默病、淀粉样蛋白、神经炎症、外周炎症、小胶质细胞、细胞因子和治疗方法。排除病例报告、未经同行评审或超过30年的文献。在考虑全文之前，先对摘要的相关性进行审查。对方法部分进行审查，以确保纳入的干预性论文为随机对照试验、荟萃分析或系统评价；然而，由于其背景信息的相关性，也纳入了几篇文献综述。基于文献综述，我们选择专注于小胶质细胞、细胞因子信号传导和外周炎症标志物。我们发现小胶质细胞激活以及随后由小胶质细胞驱动的炎症在AD的发病机制中起关键作用。此外，白细胞介素-6（IL-6）和肿瘤坏死因子-α（TNF-α）等细胞因子似乎促进淀粉样蛋白积累和细胞损伤。最后，血脑屏障（BBB）通透性增加使得外周炎症过程促进中枢神经系统（CNS）炎症和β淀粉样蛋白（Aβ）积累。目前的证据表明，免疫系统在AD的发病机制中起关键作用，无论是在中枢神经系统还是在外周。
