N-Methyl-D-Aspartate Receptors Mediate Excitotoxicity in Amyloid Beta-Induced Synaptic Pathology of Alzheimer’s Disease

Jinping Liu, Xiulai Gao, Yan Wu
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引用次数: 2

Abstract

Mounting evidence suggests that cognitive impairment begins with subtle alterations of synaptic efficacy prior to frank neuronal degeneration, and synaptic dysfunction may be induced by diffusible oligomeric assemblies of amyloid beta peptide (Aβ). The mechanisms underlying Aβ neurotoxicity are complex but might involve N-methyl-D-aspartate receptor (NMDAR). This review focuses on the action of NMDAR and its subunits in Aβ-induced synaptic dysfunction. The localized apoptotic mechanism that contributes to synaptic dysfunction in Alzheimer’s disease will also be discussed.
n -甲基- d -天冬氨酸受体介导淀粉样蛋白β诱导的阿尔茨海默病突触病理的兴奋毒性
越来越多的证据表明,认知障碍始于神经元变性之前突触功能的细微改变,突触功能障碍可能是由淀粉样β肽(Aβ)的扩散寡聚物引起的。Aβ神经毒性机制复杂,可能与n -甲基- d -天冬氨酸受体(NMDAR)有关。本文就NMDAR及其亚基在a β诱导的突触功能障碍中的作用进行综述。局部凋亡机制,有助于突触功能障碍的阿尔茨海默病也将讨论。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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