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Mitochondria as a therapeutic target in Alzheimer's disease

机译:线粒体作为阿尔茨海默氏病的治疗靶标

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摘要

Abstract 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.
机译:摘要阿尔茨海默氏病(AD)仍然是最常见的神经退行性疾病,其特征在于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,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mtDNA突变。因此线粒体可以作为AD的药物治疗靶标。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}病理中线粒体异常的最新进展,并介绍了针对线粒体的一系列药物和技术。我们认为维持线粒体功能可能为AD的治疗提供新的思路。

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