突触可塑性与阿尔茨海默病  

Synaptic plasticity and Alzheimer's disease

作　　者：陈书仪 孙洁[2] 郭爱[1] 陈沿霖 宋奇骏 邓艳秋[1] CHEN Shuyi SUN Jie GUO Ai CHEN Yanlin SONG Qijun DENG Yanqiu(IBasic Medical College, Tianjin Medical University, Tianjin 300070, Chin Department of Pathology, Tianjin People＇s Hospital, Tianjin 300070, China)

机构地区：[1]天津医科大学基础医学院病理生理教研室,天津300070 [2]天津市人民医院病理科,天津300070

出　　处：《生命的化学》2017年第4期607-611,共5页Chemistry of Life

基　　金：国家自然科学基金项目(81270422;30973156);国家级大学生创新创业训练计划(201610062013);天津医科大学基础医学院大学生科研基金(TMUUROP201603)

摘　　要：突触可塑性是指突触在神经元持续活动影响下发生的特异性数目、结构和功能的变化,它是学习记忆形成的基础,在神经功能中发挥重要的作用。突触可塑性包括突触传递和结构可塑性,二者与阿尔茨海默病(Alzheimer's disease,AD)发病有密切关系。本文从突触可塑性相关的长时程增强(longterm potentiation,LTP)、突触相关蛋白、神经递质以及神经受体和离子在AD脑内的改变,探讨突触可塑性在AD发病机制中的可能作用,为研究AD发病机制,预防和治疗提供新思路。Synaptic plasticity is a form of rapid regulation of the number, structure and function of synapse after repetitive stimulation. It is considered to be the basis of learning and memory formation and have an important role in the neural function. Synaptic plasticity includes the transmission plasticity and structure plasticity, which has a close relationship with Alzheimer＇s disease（AD）. In this review, it has been paid attention to the alterations of the long-term potentiation（LTP）, synaptic proteins, neurotransmitters, the receptors and ions in AD to explore the effects of synaptic plasticity in the physiological of AD. We hope that it will supply a new idea to investigate the pathogenesis, prevention and treatment of AD.

关 键 词：阿尔茨海默病 突触可塑性 LTP 突触相关蛋白 神经递质 NMDAR CA^2+ 

分 类 号：R749.16[医药卫生—神经病学与精神病学]