阿尔茨海默症突触功能障碍研究进展

Advances of research on synaptic dysfunction in Alzheimer's disease

阿尔茨海默症(Alzheimer’s disease,AD)是一种神经退行性疾病,以胞外β-淀粉样蛋白(amyloid-β,Aβ)沉积和胞内神经纤维缠结为病理特征。AD典型症状的出现与中枢神经系统突触数量的减少和突触功能的改变密切相关,两者主要与Aβ的神经毒性和微管结合蛋白Tau的异常修饰有关,且Aβ和Tau蛋白存在协同作用。综述了近年有关Aβ和Tau蛋白在阿尔茨海默症突触功能障碍中作用的研究进展,并总结两者的协同作用,以期为阿尔茨海默症中突触的缺失和功能障碍开发新的治疗药物。

Alzheimer＇s disease （AD） is a severe neurodegenerative disease, characterized by the presence of extracellular amyloid-β （Aβ） plaques and intracellular neurofibrillary tangles. The presence of typical AD symptoms is closely related to the decrease in the number of synapses and the change in synaptic function in the central nervous system. The changes in synaptic function are associated with neurotoxicity of Aβ and abnormal modification of microtubule binding Tau protein. This review gives a detailed discussion on the research progress in the roles of Aβ and tau proteins in synaptic dysfunction in Alzheimer＇s disease, as well as their synergistic effects, providing a reference in developing new therapeutic agents against loss and dysfunction in synapses in Alzheimer＇s disease.