Wang Jian, Chen Guo-Jun
Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing Key Laboratory of Neurology, 1 Youyi Road, Chongqing 400016, China.
Genes Dis. 2016 Jun 16;3(3):220-227. doi: 10.1016/j.gendis.2016.05.001. eCollection 2016 Sep.
Alzheimer's disease (AD) remains the most common neurodegenerative disease characterized by β-amyloid protein (Aβ) deposition and memory loss. Studies have shown that mitochondrial dysfunction plays a crucial role in AD, which involves oxidative stress-induced respiratory chain dysfunction, loss of mitochondrial biogenesis, defects of mitochondrial dynamics and mtDNA mutations. Thus mitochondria might serve as drug therapy target for AD. In this article, we first briefly discussed mitochondrial theory in the development of AD, and then we summarized recent advances of mitochondrial abnormalities in AD pathology and introduced a series of drugs and techniques targeting mitochondria. We think that maintaining mitochondrial function may provide a new way of thinking in the treatment of AD.
阿尔茨海默病(AD)仍然是最常见的神经退行性疾病,其特征是β-淀粉样蛋白(Aβ)沉积和记忆丧失。研究表明,线粒体功能障碍在AD中起关键作用,这涉及氧化应激诱导的呼吸链功能障碍、线粒体生物发生丧失、线粒体动力学缺陷和线粒体DNA突变。因此,线粒体可能成为AD的药物治疗靶点。在本文中,我们首先简要讨论了AD发展中的线粒体理论,然后总结了AD病理学中线粒体异常的最新进展,并介绍了一系列针对线粒体的药物和技术。我们认为维持线粒体功能可能为AD的治疗提供一种新的思路。