帕金森病复合体Ⅰ所致线粒体功能障碍和氧化应激的研究进展

V. N. Kumar Babu, N. Khurana
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引用次数: 1

摘要

帕金森病(PD)是一种常见的身体运动障碍,是世界上第二大进行性广泛性神经退行性疾病,据报道有1000万人患有帕金森病,占世界总人口的0.3%以上。纹状体中神经递质多巴胺(DA)的减少是这些运动症状的主要原因,统称为帕金森病。线粒体是大多数细胞中最重要的细胞器,是生命所必需的,它也被称为所有细胞代谢的心脏。线粒体的主要和最重要的作用是通过氧化磷酸化产生ATP。在这项研究中,我们将研究复杂的Ⅰ缺陷如何影响线粒体和氧化应激以及导致线粒体功能障碍的活性氧物种,我们还将研究在辅酶Q10和一些基因(如FUN-14)的帮助下治疗帕金森病的新疗法,FUNDC-1和富马酸二甲酯或BG-12在临床试验的某些阶段以及通过细胞移植治疗,未来这项研究有助于发现散发性帕金森病是如何在帕金森症中发生的。
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A Review on Mitochondrial Dysfunction and Oxidative stress due to Complex-Ⅰ in Parkinson Disease
Parkinson’s disease (PD) is the common physical movement disorder, and it is 2nd most progressive widespread neurodegenerative disorder all over the world, and it is reported that and essential 10 million, over 0.3 % of the total world population. A thoughtful reduction of the neurotransmitter dopamine (DA) in the striatum is the main cause of these motor symptoms, collectively known as parkinsonism. Mitochondria serves as most important organelle in most of the cells and are essential for life and it is also called as heart for all cellular metabolisms. The main and most important role of mitochondria is generation of ATP via oxidative phosphorylation. In this study will study about how complex Ⅰ deficiency effects the mitochondrial and oxidative stress and reactive oxygen species which cause mitochondrial dysfunction and we also study emerging therapies for Parkinson disease with the help of coenzyme Q10 and some genes like FUN-14, FUNDC-1 and dimethyl fumarate or BG-12 in some phases of clinical trials and also by cell transplantation therapy and in future this study helps in finding how this sporadic Parkinson disease occurs in parkinsonism.
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