Targeting Epac2 and GluA3-containing AMPARs:a novel therapeutic strategy for Alzheimer's disease  

作　　者：Tong Zhang Martina Schmidt 

机构地区：[1]Department of Molecular Pharmacology,Groningen Research Institute of Pharmacy,University of Groningen,Groningen,The Netherlands [2]School of Pharmacy,Tianjin Medical University,Tianjin,China

出　　处：《Neural Regeneration Research》2025年第11期3223-3224,共2页中国神经再生研究（英文版）

基　　金：supported by Alzheimer Nederland grant[WE.03-2019-05](to MS)。

摘　　要：Alzheimer's disease(AD)is a neurodegenerative disease that manifests progressive decline in memory and cognition.In the early stage of AD,memory retrieval is impaired preceding memory acquisition and consolidation(Roy et al.,2016).Prior to the onset of symptoms,pathological amyloid-β(Aβ)plagues and tau protein tangles accumulate in extracellular and intracellular spaces,respectively,leading to neurodegeneration.Among these hallmark pathologies,Aβ is proposed to be the primary etiology by triggering a cascade of pathogenic events,including neuroinflammation,oxidative stress,tau hyperphosphorylation,synaptic/neuronal dysfunction,and neuronal death(Zhang et al.,2023b).

关 键 词：ALZHEIMER IMPAIRED AΒ 

分 类 号：R749.16[医药卫生—神经病学与精神病学]