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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.

DOI:10.3390/antiox12101816
PMID:37891895
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10604635/
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/4cd2/10604635/8dc092316377/antioxidants-12-01816-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4cd2/10604635/b6e5a9372995/antioxidants-12-01816-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4cd2/10604635/faf48711b601/antioxidants-12-01816-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4cd2/10604635/8dc092316377/antioxidants-12-01816-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4cd2/10604635/b6e5a9372995/antioxidants-12-01816-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4cd2/10604635/faf48711b601/antioxidants-12-01816-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4cd2/10604635/8dc092316377/antioxidants-12-01816-g003.jpg

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本文引用的文献

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Mitochondrial damage-induced abnormal glucose metabolism with ageing in the hippocampus of APP/PS1 mice.衰老过程中线粒体损伤诱导的 APP/PS1 小鼠海马葡萄糖代谢异常。
Metabolomics. 2023 Jun 8;19(6):56. doi: 10.1007/s11306-023-02023-9.
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TG2 promotes amyloid beta aggregates: Impact on ER-mitochondria crosstalk, calcium homeostasis and synaptic function in Alzheimer's disease.转谷氨酰胺酶2促进β淀粉样蛋白聚集:对阿尔茨海默病内质网-线粒体相互作用、钙稳态及突触功能的影响
Biomed Pharmacother. 2023 Jun;162:114596. doi: 10.1016/j.biopha.2023.114596. Epub 2023 Mar 28.
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Urolithin A reduces amyloid-beta load and improves cognitive deficits uncorrelated with plaque burden in a mouse model of Alzheimer's disease.
尿石素 A 可降低阿尔茨海默病小鼠模型中的淀粉样蛋白-β负荷,并改善与斑块负担无关的认知缺陷。
Geroscience. 2023 Apr;45(2):1095-1113. doi: 10.1007/s11357-022-00708-y. Epub 2022 Dec 28.
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Upregulation of Ca-binding proteins contributes to VTA dopamine neuron survival in the early phases of Alzheimer's disease in Tg2576 mice.钙结合蛋白的上调有助于 Tg2576 小鼠阿尔茨海默病早期阶段中 VTA 多巴胺神经元的存活。
Mol Neurodegener. 2022 Nov 25;17(1):76. doi: 10.1186/s13024-022-00580-6.
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Linking the Amyloid, Tau, and Mitochondrial Hypotheses of Alzheimer's Disease and Identifying Promising Drug Targets.将阿尔茨海默病的淀粉样蛋白、tau 和线粒体假说联系起来,并确定有前途的药物靶点。
Biomolecules. 2022 Nov 11;12(11):1676. doi: 10.3390/biom12111676.
6
The effects of time-restricted eating on sleep, cognitive decline, and Alzheimer's disease.限时进食对睡眠、认知衰退和阿尔茨海默病的影响。
Exp Gerontol. 2023 Jan;171:112033. doi: 10.1016/j.exger.2022.112033. Epub 2022 Nov 17.
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