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氧化还原稳态和线粒体损伤对阿尔茨海默病的影响。

Effects of Redox Homeostasis and Mitochondrial Damage on Alzheimer's Disease.

作者信息

Wu Yi-Hsuan, Hsieh Hsi-Lung

机构信息

Research Center for Chinese Herbal Medicine, College of Human Ecology, Chang Gung University of Science and Technology, Taoyuan 333, Taiwan.

Department of Nursing, Division of Basic Medical Sciences, Graduate Institute of Health Industry Technology, Chang Gung University of Science and Technology, Taoyuan 333, Taiwan.

出版信息

Antioxidants (Basel). 2023 Sep 30;12(10):1816. doi: 10.3390/antiox12101816.

Abstract

Bioenergetic mitochondrial dysfunction is a common feature of several diseases, including Alzheimer's disease (AD), where redox imbalance also plays an important role in terms of disease development. AD is an age-related disease and begins many years before the appearance of neurodegenerative symptoms. Intracellular tau aggregation, extracellular β-amyloid (Aβ) deposition in the brain, and even the APOE4 genotype contribute to the process of AD by impairing redox homeostasis and mitochondrial dysfunction. This review summarizes the evidence for the redox imbalance and mitochondrial dysfunction in AD and demonstrates the current therapeutic strategies related to mitochondrial maintenance.

摘要

生物能量线粒体功能障碍是包括阿尔茨海默病(AD)在内的几种疾病的共同特征,在这些疾病中,氧化还原失衡在疾病发展过程中也起着重要作用。AD是一种与年龄相关的疾病,在神经退行性症状出现前许多年就开始了。细胞内tau蛋白聚集、大脑中细胞外β淀粉样蛋白(Aβ)沉积,甚至APOE4基因型,都通过损害氧化还原稳态和线粒体功能障碍,促进AD的发展进程。这篇综述总结了AD中氧化还原失衡和线粒体功能障碍的证据,并展示了目前与线粒体维持相关的治疗策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4cd2/10604635/b6e5a9372995/antioxidants-12-01816-g001.jpg

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