Oxidative stress in neurodegenerative disease: causation or association?
作者信息
Van Raamsdonk Jeremy M, Vega Irving E, Brundin Patrik
机构信息
Laboratory of Aging and Neurodegenerative Disease, Center for Neurodegenerative Science, Van Andel Research Institute, Grand Rapids, MI, USA.
Department of Translational Science and Molecular Medicine, Michigan State University, Grand Rapids, MI, USA.
出版信息
Oncotarget. 2017 Feb 14;8(7):10777-10778. doi: 10.18632/oncotarget.14650.
Abstract
摘要
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Oncotarget. 2017 Feb 14;8(7):10777-10778. doi: 10.18632/oncotarget.14650.
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本文引用的文献
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Mitochondrial dysfunction in Parkinson's disease.帕金森病中的线粒体功能障碍
J Neurochem. 2016 Oct;139 Suppl 1:216-231. doi: 10.1111/jnc.13731. Epub 2016 Aug 21.
2
Oxidative stress is increased in C. elegans models of Huntington's disease but does not contribute to polyglutamine toxicity phenotypes.在亨廷顿舞蹈症的秀丽隐杆线虫模型中氧化应激增加，但这对多聚谷氨酰胺毒性表型并无影响。
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Role of oxidative stress in Alzheimer's disease.氧化应激在阿尔茨海默病中的作用。
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Mitochondrial and cytoplasmic ROS have opposing effects on lifespan.线粒体和细胞质中的活性氧对寿命有相反的影响。
PLoS Genet. 2015 Feb 11;11(2):e1004972. doi: 10.1371/journal.pgen.1004972. eCollection 2015 Feb.
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The role of oxidative stress in Parkinson's disease.氧化应激在帕金森病中的作用。
J Parkinsons Dis. 2013;3(4):461-91. doi: 10.3233/JPD-130230.
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Alzheimer´s disease and oxidative stress: a review.阿尔茨海默病与氧化应激：综述。
Curr Med Chem. 2014;21(3):356-64. doi: 10.2174/09298673113206660258.
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Superoxide dismutase is dispensable for normal animal lifespan.超氧化物歧化酶对于正常动物寿命来说并非必不可少。
Proc Natl Acad Sci U S A. 2012 Apr 10;109(15):5785-90. doi: 10.1073/pnas.1116158109. Epub 2012 Mar 26.
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Deletion of the mitochondrial superoxide dismutase sod-2 extends lifespan in Caenorhabditis elegans.线粒体超氧化物歧化酶sod-2的缺失可延长秀丽隐杆线虫的寿命。
PLoS Genet. 2009 Feb;5(2):e1000361. doi: 10.1371/journal.pgen.1000361. Epub 2009 Feb 6.
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