{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,13]],"date-time":"2026-07-13T12:12:55Z","timestamp":1783944775485,"version":"3.55.0"},"reference-count":42,"publisher":"SAGE Publications","issue":"3","license":[{"start":{"date-parts":[[2026,3,3]],"date-time":"2026-03-03T00:00:00Z","timestamp":1772496000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,3,3]],"date-time":"2026-03-03T00:00:00Z","timestamp":1772496000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"funder":[{"DOI":"10.13039\/501100001809","name":"the National Natural Science Foundation of China","doi-asserted-by":"crossref","award":["32100762"],"award-info":[{"award-number":["32100762"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"crossref"}]},{"name":"the Shenzhen Science and Technology Program","award":["JCYJ20220530150616038"],"award-info":[{"award-number":["JCYJ20220530150616038"]}]},{"name":"the Natural Science Foundation of Guangdong Province","award":["2023A1515011707"],"award-info":[{"award-number":["2023A1515011707"]}]}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Journal of Alzheimer\u2019s Disease"],"published-print":{"date-parts":[[2026,4]]},"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by amyloid-\u03b2 plaques, neurofibrillary tangles, and synaptic dysfunction. Dysregulation of ionotropic glutamate receptors (iGluRs), including NMDA, AMPA, and kainate receptors, contributes to excitotoxicity, synaptic impairment, and cognitive decline, underscoring their therapeutic potential.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>This study aimed to conduct a comprehensive bibliometric analysis of iGluR research in AD from January 1, 1986 to August 23, 2025.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We systematically searched and analyzed the publications related to iGluRs in AD from PubMed, Web of Science, and Scopus using CiteSpace, VOSviewer, and Bibliometrix. Metrics included publication volume, citation impact, international collaborations, keyword co-occurrence, and burst detection.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      A total of 4810 papers were identified for analysis. The most prolific country, institution, journal, and author were the United States, Harvard University system,\n                      <jats:italic toggle=\"yes\">Journal of Neurochemistry<\/jats:italic>\n                      , and Lipton SA, respectively. Research has evolved from NMDAR dysfunction and A\u03b2 toxicity to clinical applications, such as memantine therapy, with recent trends focusing on AMPAR modulation and neuroprotection. Emerging researchers from China have demonstrated rapid growth. Keyword analysis reflected a sustained interest in molecular mechanisms and an increasing emphasis on clinical translation.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>This study delineates the evolution of iGluR research in AD from mechanistic insights to therapeutic innovation. While NMDARs remain central, future efforts should prioritize understudied targets like AMPARs and KARs, and leverage emerging technologies, such as cryo-electron microscopy, single-cell sequencing, and artificial intelligence, to refine therapeutic strategies and facilitate personalized medicine. It highlights targeted iGluR modulation as a promising therapeutic avenue for combating AD.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1177\/13872877261423577","type":"journal-article","created":{"date-parts":[[2026,3,11]],"date-time":"2026-03-11T10:25:00Z","timestamp":1773224700000},"page":"1365-1380","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":1,"title":["The role of ionotropic glutamate receptors in Alzheimer's disease: A scientometric analysis"],"prefix":"10.1177","volume":"110","author":[{"given":"Yunsheng","family":"Liu","sequence":"first","affiliation":[{"name":"Cancer Center, Shenzhen Hospital (Futian) of Guangzhou University of Chinese Medicine, Shenzhen, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rongde","family":"Zhong","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery, Institute of Translational Medicine, Shenzhen Second People's Hospital\/the First Affiliated Hospital of Shenzhen University Health Science Center, Shenzhen, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qian","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery, Institute of Translational Medicine, Shenzhen Second People's Hospital\/the First Affiliated Hospital of Shenzhen University Health Science Center, Shenzhen, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuyan","family":"Wang","sequence":"additional","affiliation":[{"name":"Cancer Center, Shenzhen Hospital (Futian) of Guangzhou University of Chinese Medicine, Shenzhen, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jinfang","family":"Zhang","sequence":"additional","affiliation":[{"name":"Cancer Center, Shenzhen Hospital (Futian) of Guangzhou University of Chinese Medicine, Shenzhen, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0004-8779-7186","authenticated-orcid":false,"given":"Zengwei","family":"Kou","sequence":"additional","affiliation":[{"name":"University of Toronto"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2026,3,3]]},"reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.tjpad.2025.100083"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1002\/alz.13015"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.3390\/pharmaceutics15041054"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1080\/19336950.2025.2490308"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1038\/27692"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2025.01.004"},{"key":"e_1_3_3_8_2","doi-asserted-by":"publisher","DOI":"10.3389\/fphys.2024.1446459"},{"key":"e_1_3_3_9_2","doi-asserted-by":"publisher","DOI":"10.1002\/glia.23609"},{"key":"e_1_3_3_10_2","article-title":"Molecular architecture and function mechanism of tri-heteromeric GluN1-N2-N3A NMDA receptors","volume":"14","author":"Kou Z","year":"2025","unstructured":"Kou Z, Feng Y, Zhang T, et al. 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