Yongjie Xu , Changyudong Huang , Yiqiong Zhang , Haizhi Li , Huiru Yang , Mi Liu , Liying Zhu , Chengcheng Li , Yinxue Zhong , Lei Tang , Shuyun Zhao , Wei Pan
{"title":"Diabetic encephalopathy models: A systematic review from cells to animals","authors":"Yongjie Xu , Changyudong Huang , Yiqiong Zhang , Haizhi Li , Huiru Yang , Mi Liu , Liying Zhu , Chengcheng Li , Yinxue Zhong , Lei Tang , Shuyun Zhao , Wei Pan","doi":"10.1016/j.expneurol.2025.115477","DOIUrl":null,"url":null,"abstract":"<div><div>Diabetic encephalopathy, a significant complication of diabetes, is primarily characterized by cognitive dysfunction, manifesting as deficits in learning and memory. In recent years, the global rise in diabetes prevalence has been paralleled by an increase in the incidence of diabetic encephalopathy. In some patients, this condition is further aggravated by coexisting Alzheimer's disease, leading to even more pronounced cognitive decline. Despite ongoing research, the pathogenesis of diabetic encephalopathy remains largely exploratory, and the development of targeted therapies has yet to yield significant breakthroughs. A cornerstone of disease research is the use of cell and animal models, which serve to simulate the onset and progression of various conditions. To date, over ten models have been developed for the study of diabetic encephalopathy, each offering distinct advantages and limitations, and their suitability varies depending on the research context. This review examines the current cell and animal models of diabetic encephalopathy and evaluates the rationale for model selection based on different research directions and perspectives, aiming to provide a valuable reference for advancing our understanding of the disease's pathogenesis and for facilitating drug development.</div></div>","PeriodicalId":12246,"journal":{"name":"Experimental Neurology","volume":"395 ","pages":"Article 115477"},"PeriodicalIF":4.2000,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Experimental Neurology","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0014488625003425","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
引用次数: 0
Abstract
Diabetic encephalopathy, a significant complication of diabetes, is primarily characterized by cognitive dysfunction, manifesting as deficits in learning and memory. In recent years, the global rise in diabetes prevalence has been paralleled by an increase in the incidence of diabetic encephalopathy. In some patients, this condition is further aggravated by coexisting Alzheimer's disease, leading to even more pronounced cognitive decline. Despite ongoing research, the pathogenesis of diabetic encephalopathy remains largely exploratory, and the development of targeted therapies has yet to yield significant breakthroughs. A cornerstone of disease research is the use of cell and animal models, which serve to simulate the onset and progression of various conditions. To date, over ten models have been developed for the study of diabetic encephalopathy, each offering distinct advantages and limitations, and their suitability varies depending on the research context. This review examines the current cell and animal models of diabetic encephalopathy and evaluates the rationale for model selection based on different research directions and perspectives, aiming to provide a valuable reference for advancing our understanding of the disease's pathogenesis and for facilitating drug development.
期刊介绍:
Experimental Neurology, a Journal of Neuroscience Research, publishes original research in neuroscience with a particular emphasis on novel findings in neural development, regeneration, plasticity and transplantation. The journal has focused on research concerning basic mechanisms underlying neurological disorders.