{"title":"神经胶质细胞衰老在阿尔茨海默病中的作用","authors":"Fadhl Alshaebi, Alessia Sciortino, Rakez Kayed","doi":"10.1111/jnc.70051","DOIUrl":null,"url":null,"abstract":"<p>Glial cell senescence, characterized by the irreversible arrest of cell division and a pro-inflammatory secretory phenotype, has emerged as a critical player in the pathogenesis of Alzheimer's disease (<span>ad</span>). While much attention has been devoted to the role of neurons in <span>ad</span>, growing evidence suggests that glial cells, including astrocytes, microglia, and oligodendrocytes, contribute significantly to disease progression through senescence. In this review, we explore the molecular mechanisms underlying glial cell senescence in <span>ad</span>, focusing on the cellular signaling pathways, including DNA damage response and the accumulation of senescence-associated secretory phenotypes (SASP). We also examine how senescent glial cells exacerbate neuroinflammation, disrupt synaptic function, and promote neuronal death in <span>ad</span>. Moreover, we discuss emerging therapeutic strategies aimed at targeting glial cell senescence to mitigate the neurodegenerative processes in <span>ad</span>. By providing a comprehensive overview of current research on glial cell senescence in Alzheimer's disease, this review highlights its potential as a novel therapeutic target in the fight against <span>ad</span>.\n <figure>\n <div><picture>\n <source></source></picture><p></p>\n </div>\n </figure></p>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":"169 3","pages":""},"PeriodicalIF":4.2000,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jnc.70051","citationCount":"0","resultStr":"{\"title\":\"The Role of Glial Cell Senescence in Alzheimer's Disease\",\"authors\":\"Fadhl Alshaebi, Alessia Sciortino, Rakez Kayed\",\"doi\":\"10.1111/jnc.70051\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p>Glial cell senescence, characterized by the irreversible arrest of cell division and a pro-inflammatory secretory phenotype, has emerged as a critical player in the pathogenesis of Alzheimer's disease (<span>ad</span>). While much attention has been devoted to the role of neurons in <span>ad</span>, growing evidence suggests that glial cells, including astrocytes, microglia, and oligodendrocytes, contribute significantly to disease progression through senescence. In this review, we explore the molecular mechanisms underlying glial cell senescence in <span>ad</span>, focusing on the cellular signaling pathways, including DNA damage response and the accumulation of senescence-associated secretory phenotypes (SASP). We also examine how senescent glial cells exacerbate neuroinflammation, disrupt synaptic function, and promote neuronal death in <span>ad</span>. Moreover, we discuss emerging therapeutic strategies aimed at targeting glial cell senescence to mitigate the neurodegenerative processes in <span>ad</span>. By providing a comprehensive overview of current research on glial cell senescence in Alzheimer's disease, this review highlights its potential as a novel therapeutic target in the fight against <span>ad</span>.\\n <figure>\\n <div><picture>\\n <source></source></picture><p></p>\\n </div>\\n </figure></p>\",\"PeriodicalId\":16527,\"journal\":{\"name\":\"Journal of Neurochemistry\",\"volume\":\"169 3\",\"pages\":\"\"},\"PeriodicalIF\":4.2000,\"publicationDate\":\"2025-03-25\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jnc.70051\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Neurochemistry\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://onlinelibrary.wiley.com/doi/10.1111/jnc.70051\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"BIOCHEMISTRY & MOLECULAR BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Neurochemistry","FirstCategoryId":"3","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1111/jnc.70051","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
The Role of Glial Cell Senescence in Alzheimer's Disease
Glial cell senescence, characterized by the irreversible arrest of cell division and a pro-inflammatory secretory phenotype, has emerged as a critical player in the pathogenesis of Alzheimer's disease (ad). While much attention has been devoted to the role of neurons in ad, growing evidence suggests that glial cells, including astrocytes, microglia, and oligodendrocytes, contribute significantly to disease progression through senescence. In this review, we explore the molecular mechanisms underlying glial cell senescence in ad, focusing on the cellular signaling pathways, including DNA damage response and the accumulation of senescence-associated secretory phenotypes (SASP). We also examine how senescent glial cells exacerbate neuroinflammation, disrupt synaptic function, and promote neuronal death in ad. Moreover, we discuss emerging therapeutic strategies aimed at targeting glial cell senescence to mitigate the neurodegenerative processes in ad. By providing a comprehensive overview of current research on glial cell senescence in Alzheimer's disease, this review highlights its potential as a novel therapeutic target in the fight against ad.
期刊介绍:
Journal of Neurochemistry focuses on molecular, cellular and biochemical aspects of the nervous system, the pathogenesis of neurological disorders and the development of disease specific biomarkers. It is devoted to the prompt publication of original findings of the highest scientific priority and value that provide novel mechanistic insights, represent a clear advance over previous studies and have the potential to generate exciting future research.