摘要
阿尔茨海默病(Alzheimer’s disease,AD)是以β淀粉样蛋白(amyloidβ,Aβ)沉积和神经纤维缠结(neurofibrillary tangles,NFTs)等病理特征及记忆衰退等临床特征为标志的一种神经退行性疾病。AD的主要症状认知障碍与突触减少密切相关。可溶性寡聚Aβ引起的突触功能损伤是AD早期病理机制研究的热点。星形胶质细胞对突触功能调控起重要作用,其功能改变与AD病理表现密切相关。星形胶质细胞可以通过参与Aβ代谢、中枢炎性反应、突触调控和胞内钙信号传递等途径参与AD早期的突触功能损伤。该文对近年来星形胶质细胞在AD早期突触功能损伤中的主要作用及机制进行综述,同时对这一领域的开放问题进行了归纳。
Alzheimer’s disease(AD),a neurodegenerative disease,is characterized by the presence of extracellular amyloid-β(Aβ)aggregates and intracellular neurofibrillary tangles formed by hyperphosphorylated tau as pathological features and the cognitive decline as main clinical feature.An important cellular correlation of cognitive decline in AD is synapse loss.Soluble Aβoligomer has been proposed to be a crucial early event leading to synapse dysfunction in AD.Astrocytes are crucial for synaptic formation and function,and defects in astrocytic activation and function have been suggested in the pathogenesis of AD.Astrocytes may contribute to synapse dysfunction at an early stage of AD by participating in Aβmetabolism,brain inflammatory response,synaptic regulation,and intracellular calcium signaling.In this review,we describe the role of astrocytes and underlying mechanisms in regulating synapse dysfunction in early AD,and discuss the open questions in this field.
作者
刘聪
沈逸
LIU Cong;SHEN Yi(Department of Neurobiology,Zhejiang University School of Medicine,Hangzhou 310058,China)
出处
《生命科学》
CSCD
北大核心
2021年第8期946-954,共9页
Chinese Bulletin of Life Sciences
基金
国家自然科学基金项目(81971139)
中央高校基本科研业务费专项资金项目(2019FZA7004)。
