Amyloid-beta pathology-induced nanoscale synaptic disruption:the case of the GABA_B-GIRK assembly  

作　　者：Rafael Lujan Alejandro Martín-Belmonte Sergi Ferré Francisco Ciruela 

机构地区：[1]Synaptic Structure Laboratory,Instituto de Biomedicina de la UCLM(IB-UCLM),Departamento de Ciencias Médicas,Instituto de Investigación en Salud de Castilla-La Mancha(IDISCAM),Facultad de Medicina,Universidad Castilla-La Mancha,Campus Biosanitario,C/Almansa,Albacete,Spain [2]Integrative Neurobiology Section,National Institute on Drug Abuse,Intramural Research Program,National Institutes of Health,Baltimore,MD,USA [3]Pharmacology Unit,Department of Pathology and Experimental Therapeutics,School of Medicine and Health Sciences,Institute of Neurosciences,University of Barcelona,Neuropharmacology&Pain Group,Neuroscience Program,Bellvitge Institute for Biomedical Research,L’Hospitalet de Llobregat,Spain

出　　处：《Neural Regeneration Research》2025年第5期1409-1410,共2页中国神经再生研究（英文版）

摘　　要：Alzheimer's disease (AD) is characterized by an imbalance between excitatory and inhibitory brain networks,leading to aberrant homeostatic synaptic plasticity.AD has progressively been recognized as syna ptopathy and syna ptic dysfunction has been identified as a key component of its pathogenesis (Schirinzi et al.,2020).Syna ptic dysfunction is believed to precede synapse loss,a primary biological correlate of cognitive decline in AD,inevita bly associated with neuronal death.

关 键 词：ALZHEIMER PATHOLOGY 

分 类 号：R749.16[医药卫生—神经病学与精神病学]