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多走(突触)一步:兴奋性毒性作为通往神经退行性疾病之路

Going the Extra (Synaptic) Mile: Excitotoxicity as the Road Toward Neurodegenerative Diseases.

作者信息

Armada-Moreira Adam, Gomes Joana I, Pina Carolina Campos, Savchak Oksana K, Gonçalves-Ribeiro Joana, Rei Nádia, Pinto Sara, Morais Tatiana P, Martins Robertta Silva, Ribeiro Filipa F, Sebastião Ana M, Crunelli Vincenzo, Vaz Sandra H

机构信息

Instituto de Farmacologia e Neurociências, Faculdade de Medicina da Universidade de Lisboa, Lisbon, Portugal.

Instituto de Medicina Molecular João Lobo Antunes, Faculdade de Medicina da Universidade de Lisboa, Lisbon, Portugal.

出版信息

Front Cell Neurosci. 2020 Apr 24;14:90. doi: 10.3389/fncel.2020.00090. eCollection 2020.

Abstract

Excitotoxicity is a phenomenon that describes the toxic actions of excitatory neurotransmitters, primarily glutamate, where the exacerbated or prolonged activation of glutamate receptors starts a cascade of neurotoxicity that ultimately leads to the loss of neuronal function and cell death. In this process, the shift between normal physiological function and excitotoxicity is largely controlled by astrocytes since they can control the levels of glutamate on the synaptic cleft. This control is achieved through glutamate clearance from the synaptic cleft and its underlying recycling through the glutamate-glutamine cycle. The molecular mechanism that triggers excitotoxicity involves alterations in glutamate and calcium metabolism, dysfunction of glutamate transporters, and malfunction of glutamate receptors, particularly N-methyl-D-aspartic acid receptors (NMDAR). On the other hand, excitotoxicity can be regarded as a consequence of other cellular phenomena, such as mitochondrial dysfunction, physical neuronal damage, and oxidative stress. Regardless, it is known that the excessive activation of NMDAR results in the sustained influx of calcium into neurons and leads to several deleterious consequences, including mitochondrial dysfunction, reactive oxygen species (ROS) overproduction, impairment of calcium buffering, the release of pro-apoptotic factors, among others, that inevitably contribute to neuronal loss. A large body of evidence implicates NMDAR-mediated excitotoxicity as a central mechanism in the pathogenesis of many neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS), Alzheimer's disease (AD), and epilepsy. In this review article, we explore different causes and consequences of excitotoxicity, discuss the involvement of NMDAR-mediated excitotoxicity and its downstream effects on several neurodegenerative disorders, and identify possible strategies to study new aspects of these diseases that may lead to the discovery of new therapeutic approaches. With the understanding that excitotoxicity is a common denominator in neurodegenerative diseases and other disorders, a new perspective on therapy can be considered, where the targets are not specific symptoms, but the underlying cellular phenomena of the disease.

摘要

兴奋性毒性是一种描述兴奋性神经递质(主要是谷氨酸)毒性作用的现象,其中谷氨酸受体的过度激活或持续激活引发一系列神经毒性反应,最终导致神经元功能丧失和细胞死亡。在这个过程中,正常生理功能与兴奋性毒性之间的转变很大程度上由星形胶质细胞控制,因为它们能够控制突触间隙中谷氨酸的水平。这种控制是通过从突触间隙清除谷氨酸及其通过谷氨酸-谷氨酰胺循环进行的基础再循环来实现的。引发兴奋性毒性的分子机制涉及谷氨酸和钙代谢的改变、谷氨酸转运体功能障碍以及谷氨酸受体(特别是N-甲基-D-天冬氨酸受体,NMDAR)功能异常。另一方面,兴奋性毒性可被视为其他细胞现象的结果,如线粒体功能障碍、物理性神经元损伤和氧化应激。无论如何,已知NMDAR的过度激活会导致钙持续流入神经元,并引发多种有害后果,包括线粒体功能障碍、活性氧(ROS)过度产生、钙缓冲受损、促凋亡因子释放等,这些都不可避免地导致神经元丢失。大量证据表明,NMDAR介导的兴奋性毒性是许多神经退行性疾病(包括肌萎缩侧索硬化症(ALS)、阿尔茨海默病(AD)和癫痫)发病机制的核心机制。在这篇综述文章中,我们探讨了兴奋性毒性的不同原因和后果,讨论了NMDAR介导的兴奋性毒性及其对几种神经退行性疾病的下游影响,并确定了研究这些疾病新方面的可能策略,这些策略可能会导致发现新的治疗方法。鉴于兴奋性毒性是神经退行性疾病和其他疾病的共同特征,可以考虑一种新的治疗视角,即治疗靶点不是特定症状,而是疾病潜在的细胞现象。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/26fe/7194075/33dfb882873c/fncel-14-00090-g0001.jpg

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