Amyloid-beta and mitochondria in aging and Alzheimer's disease: implications for synaptic damage and cognitive decline.
Amyloid-beta and mitochondria in aging and Alzheimer's disease: implications for synaptic damage and cognitive decline.
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DOI：
10.3233/jad-2010-100504
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发表时间：
2010
期刊：
影响因子：
--
通讯作者：
Shirendeb U
中科院分区：
文献类型：
--
作者：
Reddy PH;Manczak M;Mao P;Calkins MJ;Reddy AP;Shirendeb U
本文综述了淀粉样蛋白(Aβ，Aβ)和线粒体在阿尔茨海默病(AD)患者突触损伤和认知功能减退中的作用。最近的分子、细胞、动物模型和死后脑研究表明，Aβ和线粒体异常是导致AD突触损伤和认知功能下降的关键因素。据报道，β积聚在亚细胞室，损害AD患者神经元的正常功能。此外，最近使用生化方法和电子显微镜的研究表明，Aβ在神经末梢的积累影响突触活动，包括神经递质和突触小泡的释放。最近对AD患者线粒体与Aβ关系的研究表明，在线粒体中，Aβ引起的结构改变导致线粒体碎裂增加，线粒体融合减少，线粒体功能障碍和突触损伤。本文就Aβ、线粒体、脑内AD的年龄依赖性因素以及AD的突触损伤等方面的最新研究进展作一综述。本文还简要讨论了线粒体疗法在AD患者治疗中的潜在作用。
This article reviews the role of amyloid-β (Aβ) and mitochondria in synaptic damage and cognitive decline found in patients with Alzheimer’s disease (AD). Recent molecular, cellular, animal model, and postmortem brain studies have revealed that Aβ and mitochondrial abnormalities are key factors that cause synaptic damage and cognitive decline in AD. Aβ is reported to accumulate in subcellular compartments and to impair the normal function of neurons in AD patients. Further, recent studies using biochemical methods and electron microscopy have revealed that the accumulation of Aβ at nerve terminals affect synaptic activities, including the release of neurotransmitters and synaptic vesicles. Recent studies of the relationship between mitochondria and Aβ in AD patients suggest that in mitochondria, structural changes caused by Aβ result in increased mitochondrial fragmentation, decreased mitochondrial fusion, mitochondrial dysfunction, and synaptic damage. This paper discusses the latest research on Aβ, mitochondria, age-dependent factors of AD in the brain, and synaptic damage in AD. This paper also briefly discusses potential mitochondrial therapeutics in the treatment of patients with AD.