p38-MAPK and CDK5,signaling pathways in neuroinflammation:a potential therapeutic intervention in Alzheimer's disease?  

作　　者：Vlad Ionut Viorel Ylenia Pastorello Nosherwan Bajwa Mark Slevin 

机构地区：[1]George Emil Palade University of Medicine,Pharmacy,Science and Technology,Târgu Mures,Romania [2]Department of Anatomy and Embryology,George Emil Palade University of Medicine,Pharmacy,Science and Technology,Targu Mures,Romania [3]DIAKO Hospital,Flensburg,Germany [4]Center for Advanced Medical and Pharmaceutical Research(CCAMF),George Emil Palade University of Medicine,Pharmacy,Science and Technology,Târgu Mures,Romania [5]Manchester Metropolitan University,Manchester,UK

出　　处：《Neural Regeneration Research》2024年第8期1649-1650,共2页中国神经再生研究(英文版)

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 characte rized by the build-up of amyloid-beta(Aβ)plaques and neurofibrillary to ngles containing hyperphosphorylated tau protein.

关 键 词：ALZHEIMER AΒ TAU 

分 类 号：R749.16[医药卫生—神经病学与精神病学]