p38-MAPK and CDK5,signaling pathways in neuroinflammation:a potential therapeutic intervention in Alzheimer's disease?
Vlad Ionut Viorel1
Ylenia Pastorello2
Nosherwan Bajwa3
Mark Slevin4
1.George Emil Palade University of Medicine,Pharmacy,Science and Technology,Târgu Mures,Romania2.Department of Anatomy and Embryology,George Emil Palade University of Medicine,Pharmacy,Science and Technology,Târgu Mures,Romania3.DIAKO Hospital,Flensburg,Germany4.Center for Advanced Medical and Pharmaceutical Research(CCAMF),George Emil Palade University of Medicine,Pharmacy,Science and Technology,Târgu Mures,Romania;Manchester Metropolitan University,Manchester,UK
摘要：Alzheimer's disease(AD),the most common type of dementia,affects millions of people worldwide,putting a significant strain on healthcare infrastructure and societal resources.AD is characterized by the build-up of amyloid-beta(Aβ)plaques and neurofibrillary tangles containing hyperphosphorylated tau protein.These pathological features cause neuroinflammation,vascular dysfunction,and ultimately,neuronal death and cognitive decline(Long and Holtzman,2019).Two critical signaling pathways,the mitogen-activated protein kinase(MAPK)family and cyclin-dependent kinase 5(CDK5),have been implicated in the pathogenesis of AD.There are three primary subfamilies within the MAPK family,namely extracellular signal-regulated kinases,c-Jun N-terminal kinases,and p38 MAPKs.
机标关键词：p38-mapkalzheimerpathwaysdiseaseeuroinflammationinterventionpotential
论文发表日期：2024-08-28
在线出版日期：2025-08-15（本平台首次上网日期，不代表文献的发表时间）
页数：2( 1649-1650 )