摘要
主要的神经退行性疾病,如阿尔茨海默氏病(AD)和帕金森病(PD)的病因仍然是未知的,但越来越多的证据表明,谷氨酸和线粒体两个突出的球员在氧化应激(OS)的过程是这些疾病的基础。虽然阿尔茨海默病和帕金森病有明显的病理和临床特点,但氧化应激是一种常见的机制能导致神经元损伤。谷氨酸是一种重要的神经递质和神经胶质细胞,并且它强烈依赖于钙稳态和线粒体功能。在目前的工作中,我们专注于谷氨酸诱导的钙信号和细胞死亡过程中的线粒体功能障碍的关系。此外,我们已经讨论了这一途径的的改变如何可能导致或加剧的神经退行性疾病。最后,这篇综述的目的是刺激进一步研究这个问题,从而从一个新的角度来看可能的治疗药物的设计或生物标志物的识别。
关键词: 阿尔茨海默病,谷氨酸,氧化应激,帕金森病,线粒体。
Current Alzheimer Research
Title:Glutamate and Mitochondria: Two Prominent Players in the Oxidative Stress-Induced Neurodegeneration
Volume: 13 Issue: 2
Author(s): Tommaso Cassano, Lorenzo Pace, Gaurav Bedse, Angelo Michele Lavecchia, Federico De Marco, Silvana Gaetani and Gaetano Serviddio
Affiliation:
关键词: 阿尔茨海默病,谷氨酸,氧化应激,帕金森病,线粒体。
摘要: The aetiology of major neurodegenerative diseases such as Alzheimer’s disease (AD) and Parkinson’s disease (PD) is still unknown, but increasing evidences suggest that glutamate and mitochondria are two prominent players in the oxidative stress (OS) process that underlie these illnesses. Although AD and PD have distinct pathological and clinical features, OS is a common mechanism contributing to neuronal damage. Glutamate is an important neurotransmitter in neurons and glial cells and is strongly dependent on calcium homeostasis and on mitochondrial function. In the present work we focused on glutamate- induced calcium signaling and its relation to the mitochondrial dysfunction with cell death processes. In addition, we have discussed how alterations in this pathway may lead or aggravate the neurodegenerative diseases. Finally, this review aims to stimulate further studies on this issue and thereby engage a new perspective regarding the design of possible therapeutic agents or the identification of biomarkers.
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Tommaso Cassano, Lorenzo Pace, Gaurav Bedse, Angelo Michele Lavecchia, Federico De Marco, Silvana Gaetani and Gaetano Serviddio , Glutamate and Mitochondria: Two Prominent Players in the Oxidative Stress-Induced Neurodegeneration, Current Alzheimer Research 2016; 13 (2) . https://dx.doi.org/10.2174/1567205013666151218132725
DOI https://dx.doi.org/10.2174/1567205013666151218132725 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
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