{"title":"Bibliometric analysis of pathological mechanisms in Alzheimer's disease: Applications based on mouse models.","authors":"Jinjiang Li, Zhaoxiong Lin, Yufei Niu, Wenrui Chang, Siyun Song, Guang Yang, Feng Liu, Jiaxin Dai, Chunyan Hao","doi":"10.1177/25424823251367046","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Alzheimer's disease (AD) is a progressive neurodegenerative disorder marked by memory loss and cognitive decline. Animal models play a key role in exploring its pathophysiological mechanisms.</p><p><strong>Objective: </strong>To analyze global research trends and knowledge structure in AD pathophysiological mechanisms based on animal models.</p><p><strong>Methods: </strong>Publications from 2014 to 2023 were retrieved from the Web of Science Core Collection. CiteSpace and VOSviewer were used for bibliometric analysis and data visualization.</p><p><strong>Results: </strong>A total of 2169 publications were identified, with a steady growth trend. The United States and China were the leading contributors, with Harvard University as a major collaborative hub. The Journal of Alzheimer's Disease published the most articles, while the Journal of Neuroscience had the highest co-citation frequency. Holtzman DM was a key author in the field. Nine keyword clusters were identified, including insulin resistance, amyloid beta, and oxidative stress. Emerging topics include synapse loss, gut microbiota, and NLRP3 inflammasome.</p><p><strong>Conclusions: </strong>This study provides a concise overview of global research on AD pathophysiological mechanisms in animal models, offering valuable insights for future research directions.</p>","PeriodicalId":73594,"journal":{"name":"Journal of Alzheimer's disease reports","volume":"9 ","pages":"25424823251367046"},"PeriodicalIF":2.8000,"publicationDate":"2025-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12351105/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Alzheimer's disease reports","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1177/25424823251367046","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/1 0:00:00","PubModel":"eCollection","JCR":"Q2","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
引用次数: 0
Abstract
Background: Alzheimer's disease (AD) is a progressive neurodegenerative disorder marked by memory loss and cognitive decline. Animal models play a key role in exploring its pathophysiological mechanisms.
Objective: To analyze global research trends and knowledge structure in AD pathophysiological mechanisms based on animal models.
Methods: Publications from 2014 to 2023 were retrieved from the Web of Science Core Collection. CiteSpace and VOSviewer were used for bibliometric analysis and data visualization.
Results: A total of 2169 publications were identified, with a steady growth trend. The United States and China were the leading contributors, with Harvard University as a major collaborative hub. The Journal of Alzheimer's Disease published the most articles, while the Journal of Neuroscience had the highest co-citation frequency. Holtzman DM was a key author in the field. Nine keyword clusters were identified, including insulin resistance, amyloid beta, and oxidative stress. Emerging topics include synapse loss, gut microbiota, and NLRP3 inflammasome.
Conclusions: This study provides a concise overview of global research on AD pathophysiological mechanisms in animal models, offering valuable insights for future research directions.
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