Mapping microglial mechanisms in Alzheimer's disease: a comprehensive analysis

Microglia, the brain's primary immune cells, play crucial roles in Alzheimer's disease (AD) pathogenesis. However, existing research remains abundant yet fragmented. Therefore, this study aimed to systematically identify hotspots and trends in microglia-related AD research, while providing an in-depth analysis of the underlying mechanisms to advance mechanistic understanding and therapeutic development. To achieve this, articles on microglia in AD were retrieved from the Web of Science Core Collection (WoSCC) database, and bibliometric analysis was performed using the WoSCC platform and CiteSpace 6.3.R1, with a focus on global collaboration, institutional and journal contributions, keyword bursts, and high-impact articles to comprehensively elucidate the underlying mechanisms. In total, 1,043 articles from 67 countries and regions were included.Among them, the United States led with 484 articles and an H-index of 100, followed by China with 276 articles. The University of California system (77 articles) and Harvard University (74 articles) had the highest H-index, both at 41. Journal of Neuroinflammation published the most articles (57 articles). Burst keywords persisting until 2024 included "memory," "NLRP3 inflammasome," and "system." High-impact studies emphasized microglial roles in AD pathology, including Aβ clearance, synaptic pruning, inflammation, metabolism, phenotype shifts, immune memory, and genetic variation. Overall, microglial mechanisms are at the forefront of AD research. The United States leads in both article number and influence, followed by China. The University of California system and Harvard University demonstrate the greatest output and impact. Journal of Neuroinflammation is the leading journal. Microglial NLRP3 activation, system-level interactions, and memory impairment have emerged as key research hotspots in AD. Future research will focus on microglial mechanisms and therapeutic targets in AD.