摘要
目前对阿尔茨海默病(AD)的分子理解尚未导致成功的干预。目前,AD大脑的线粒体功能障碍正成为这种疾病的一个标志。AD中经常影响的一个线粒体功能是氧化磷酸化,负责ATP的产生,也负责活性氧(ROS)的产生和嘧啶的从头合成。本文综述了线粒体产生的活性氧和嘧啶在AD发病机制中的作用及其在大分子氧化变性、必需磷脂合成和维持AD脑线粒体活性中的作用。
关键词: 线粒体,DNA修复,dNTP池,核苷酸代谢,大脑
Current Medicinal Chemistry
Title:The Role of Mitochondrial Dysfunction in the Progression of Alzheimer’s Disease
Volume: 25 Issue: 40
关键词: 线粒体,DNA修复,dNTP池,核苷酸代谢,大脑
摘要: The current molecular understanding of Alzheimer’s disease (AD) has still not resulted in successful interventions. Mitochondrial dysfunction of the AD brain is currently emerging as a hallmark of this disease. One mitochondrial function often affected in AD is oxidative phosphorylation responsible for ATP production, but also for production of reactive oxygen species (ROS) and for the de novo synthesis of pyrimidines. This paper reviews the role of mitochondrial produced ROS and pyrimidines in the aetiology of AD and their proposed role in oxidative degeneration of macromolecules, synthesis of essential phospholipids and maintenance of mitochondrial viability in the AD brain.
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Cite this article as:
The Role of Mitochondrial Dysfunction in the Progression of Alzheimer’s Disease, Current Medicinal Chemistry 2018; 25 (40) . https://dx.doi.org/10.2174/0929867324666170616110111
DOI https://dx.doi.org/10.2174/0929867324666170616110111 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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