老年痴呆症中神经递质释放异常的机理  

Abnormal neurotransmitter release in Alzheimer's disease

作　　者：何洋[1] 周煜东 

机构地区：[1]浙江大学医学部神经科学研究所,卫生部医学神经生物学重点实验室,浙江省神经生物学重点实验室,杭州310058

出　　处：《生命科学》2014年第1期27-34,共8页Chinese Bulletin of Life Sciences

基　　金：国家重点基础研究发展计划("973"项目)(2013CB530902);国家自然科学基金项目(91132712;81221003);浙江省自然科学基金项目(LR12C09001)

摘　　要：阿尔茨海默症(Alzheimer’s disease,AD)是以胞外淀粉样蛋白(amyloid-β,Aβ)沉积和胞内神经纤维缠结为病理特征的神经退行性疾病。AD典型症状的出现与中枢神经系统突触数量的减少密切相关,因此,明确AD早期突触数量还没有明显降低时突触功能失调的机制对AD的临床诊治具有十分重要的意义。寡聚Aβ、早老素功能缺失等因素造成的突触前神经递质释放异常很有可能是AD突触功能异常的上游机制。对AD中神经递质释放异常的现象和机制进行综述,并对这一领域存在的开放问题作一归纳。Alzheimer＇s disease （AD） is a severe neurodegenerative disease that is characterized by the presence of extracellular amyloid-β （Aβ） plaques and intracellular neurofibrillary tangles. Synapse loss is the best pathological correlate of typical AD symptoms, but once synapse loss is observed in patients with AD, its progression is hard to be stopped. Thus, elucidating synapse dysfunction before the occurrence of central synapse loss is of particular importance to the diagnosis and treatment of AD. Aberrant neurotransmitter release, caused by Aβ oligomers, loss- of-function presenilin mutations, etc, is possibly a promising upstream mechanism of synapse dysfunction. In this review, we first describe presynaptic transmitter release abnormalities and underlying mechanisms in AD, and then raise a few key open questions in the research field.

关 键 词：阿尔茨海默症 神经递质释放 Β淀粉样蛋白 早老素 突触囊泡 

分 类 号：Q42[生物学—神经生物学] R749.16[生物学—生理学]