Ferroptosis in Alzheimer's Disease: Integrating Bibliometric Analysis and Bioinformatic Insights to Identify Emerging Research Frontiers (2012–2026)

Alzheimer's disease (AD) is the leading cause of dementia worldwide and represents a major unmet clinical challenge. Emerging evidence suggests that ferroptosis, an iron-dependent form of regulated cell death characterized by lipid peroxidation and oxidative stress, plays a pivotal role in the pathogenesis of AD by linking iron dyshomeostasis, mitochondrial dysfunction, neuroinflammation, and amyloid-β and tau pathology. Despite the rapid growth of research in this area, the global knowledge structure, evolving research priorities, and molecular mechanisms underlying ferroptosis in AD remain fragmented and insufficiently integrated.

This project aims to combine bibliometric and scientometric approaches with bioinformatic analyses to comprehensively map the research landscape and identify emerging molecular targets in ferroptosis-related Alzheimer's disease research from 2012 to 2026. Bibliographic data retrieved from PubMed, Scopus, and Web of Science will be analyzed using VOSviewer, CiteSpace, and Bibliometrix to evaluate publication trends, collaborative networks, co-citation patterns, and thematic evolution. To complement these analyses, ferroptosis-associated gene sets from FerrDb will be integrated with publicly available transcriptomic datasets from GEO and AMP-AD to identify differentially expressed genes, enriched biological pathways, protein-protein interaction networks, and cell type-specific ferroptosis signatures. By synthesizing quantitative research trends with molecular evidence, this study seeks to uncover knowledge gaps, prioritize candidate biomarkers and therapeutic targets, and provide actionable insights for future translational and precision medicine approaches in Alzheimer's disease.