Nada H Aljarba, Hayder M Al-Kuraishy, Ali I Al-Gareeb, Mustafa M Shokr, Marios Papadakis, Athanasios Alexiou, Mubarak Alruwaili, Mohammed Alrouji, Mohammed S Alshammari, Gaber El-Saber Batiha
{"title":"The possible therapeutic role of advanced glycation end-product inhibitors in ischemic stroke.","authors":"Nada H Aljarba, Hayder M Al-Kuraishy, Ali I Al-Gareeb, Mustafa M Shokr, Marios Papadakis, Athanasios Alexiou, Mubarak Alruwaili, Mohammed Alrouji, Mohammed S Alshammari, Gaber El-Saber Batiha","doi":"10.1016/j.brainresbull.2025.111236","DOIUrl":null,"url":null,"abstract":"<p><p>The advanced glycation end-products (AGEs) are toxic molecules result from non-enzymatic interactions of sugar with lipids or proteins. AGEs promote the generation of reactive oxygen species that induce the release of pro-inflammatory cytokines, and alter the intracellular signaling leading to progressive biochemical and metabolic derangements. AGEs-induced cellular aging is implicated in the development and progression of different neurological disorders such as dementia, neuropsychiatric disorders, and cerebrovascular diseases. Particularly, AGEs-induced microangiopathy and macroangiopathy trigger the induction of prothrombotic/thrombotic cascades with subsequent increase risk of acute ischemic stroke (AIS). Many studies highlighted that AGEs serum levels are correlated with the incidence, pathogenicity, and severity of AIS. However, the relationship between AGEs and AIS is not elucidated completely. Therefore, this review aims to discuss how AGEs promote the development and progression of AIS, and how AGEs inhibitors could be effective in the management of AIS.</p>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":" ","pages":"111236"},"PeriodicalIF":3.5000,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Brain Research Bulletin","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1016/j.brainresbull.2025.111236","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
引用次数: 0
Abstract
The advanced glycation end-products (AGEs) are toxic molecules result from non-enzymatic interactions of sugar with lipids or proteins. AGEs promote the generation of reactive oxygen species that induce the release of pro-inflammatory cytokines, and alter the intracellular signaling leading to progressive biochemical and metabolic derangements. AGEs-induced cellular aging is implicated in the development and progression of different neurological disorders such as dementia, neuropsychiatric disorders, and cerebrovascular diseases. Particularly, AGEs-induced microangiopathy and macroangiopathy trigger the induction of prothrombotic/thrombotic cascades with subsequent increase risk of acute ischemic stroke (AIS). Many studies highlighted that AGEs serum levels are correlated with the incidence, pathogenicity, and severity of AIS. However, the relationship between AGEs and AIS is not elucidated completely. Therefore, this review aims to discuss how AGEs promote the development and progression of AIS, and how AGEs inhibitors could be effective in the management of AIS.
期刊介绍:
The Brain Research Bulletin (BRB) aims to publish novel work that advances our knowledge of molecular and cellular mechanisms that underlie neural network properties associated with behavior, cognition and other brain functions during neurodevelopment and in the adult. Although clinical research is out of the Journal''s scope, the BRB also aims to publish translation research that provides insight into biological mechanisms and processes associated with neurodegeneration mechanisms, neurological diseases and neuropsychiatric disorders. The Journal is especially interested in research using novel methodologies, such as optogenetics, multielectrode array recordings and life imaging in wild-type and genetically-modified animal models, with the goal to advance our understanding of how neurons, glia and networks function in vivo.