Global research architecture of RNA-binding proteins in neurodegenerative diseases: a web of science bibliometric study with PubMed record verification, 2001-2025.

Background: RNA-binding proteins (RBPs) connect RNA homeostasis to proteostasis and selective neuronal vulnerability, but the organization and evolution of this cross-disease research field remain unclear. Methods: We analyzed Web of Science Core Collection (WoSCC) records published through 2025. PubMed was used only to verify records by normalized DOI or exact normalized title; PubMed metadata were not pooled with WoS data, and all bibliometric analyses used WoS fields. Publication growth, contributors, collaboration, co-citation, bibliographic coupling, and conceptual evolution were examined using bibliometrix, VOSviewer, and CiteSpace-compatible workflows. A prespecified 43-concept dictionary preserved multiword biological entities in title/abstract networks. The study characterizes a query-defined and PubMed-verified literature corpus rather than estimating the relative biological importance of individual RBPs. Results: Of 2,454 records reported by the WoS search interface, 2,450 were available in the supplied exports and 2,309 met the year criterion. PubMed record verification retained 2,160 records (93.55%) in the analysis corpus; 149 records (6.45%) were not matched. Output increased from one publication in 2001 to 213 in 2025. Within this query-defined corpus, the mapped literature was concentrated around TDP-43 pathology, TARDBP/FUS genetics, and loss of RNA-processing function. The controlled concept network resolved three macro-communities, while recent temporal signals involved LATE, cryptic exons, and RNA transport. These findings describe the retrieved and verified corpus and are not presented as a search-independent ranking of the broader RBP field. Conclusion: The maps document a WoS-derived and PubMed-verified literature corpus concentrated on TDP-43 and ALS/FTD and increasingly connected with cryptic RNA processing, condensate biology, nuclear transport, neuroimmune responses, and aging-related mixed proteinopathies. Because the corpus was conditioned by a title-level query containing named RBPs and by PubMed record verification, these patterns should not be interpreted as an unbiased ranking of RBP biology or as evidence of shared causality across diseases. Cross-disease translation should proceed through neuropathologically defined, age-stratified, and cell-type-resolved human cohorts, followed by causal perturbation and rescue in human disease models and multicenter longitudinal validation.