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线粒体与神经炎症之间的关系:对阿尔茨海默病的影响

Relationships Between Mitochondria and Neuroinflammation: Implications for Alzheimer's Disease.

作者信息

Wilkins Heather M, Swerdlow Russell H

机构信息

University of Kansas School of Medicine, MS 2012, Landon Center on Aging, 3901 Rainbow Boulevard, Kansas City, KS 66160, USA.

出版信息

Curr Top Med Chem. 2016;16(8):849-57. doi: 10.2174/1568026615666150827095102.

Abstract

Mitochondrial dysfunction and neuroinflammation occur in Alzheimer's disease (AD). The causes of these pathologic lesions remain uncertain, but links between these phenomena are increasingly recognized. In this review, we discuss data that indicate mitochondria or mitochondrial components may contribute to neuroinflammation. While mitochondrial dysfunction could cause neuroinflammation, neuroinflammation could also cause mitochondrial dysfunction. However, based on the systemic nature of AD mitochondrial dysfunction as well as data from experiments we discuss, the former possibility is perhaps more likely. If correct, then manipulation of mitochondria, either directly or through manipulations of bioenergetic pathways, could prove effective in reducing metabolic dysfunction and neuroinflammation in AD patients. We also review some potential approaches through which such manipulations may be achieved.

摘要

线粒体功能障碍和神经炎症在阿尔茨海默病(AD)中都会出现。这些病理损伤的原因尚不确定,但人们越来越认识到这些现象之间的联系。在这篇综述中,我们讨论了表明线粒体或线粒体成分可能导致神经炎症的数据。虽然线粒体功能障碍可能导致神经炎症,但神经炎症也可能导致线粒体功能障碍。然而,基于AD线粒体功能障碍的系统性本质以及我们所讨论的实验数据,前一种可能性或许更大。如果这是正确的,那么直接或通过对生物能量途径的调控来操纵线粒体,可能会被证明对减轻AD患者的代谢功能障碍和神经炎症有效。我们还综述了一些可能实现这种调控的潜在方法。

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本文引用的文献

2
Cytoplasmic hybrid (cybrid) cell lines as a practical model for mitochondriopathies.
Redox Biol. 2014;2:619-31. doi: 10.1016/j.redox.2014.03.006. Epub 2014 Apr 1.
3
Bioenergetic dysfunction and inflammation in Alzheimer's disease: a possible connection.
Front Aging Neurosci. 2014 Nov 10;6:311. doi: 10.3389/fnagi.2014.00311. eCollection 2014.
4
Effect of one month duration ketogenic and non-ketogenic high fat diets on mouse brain bioenergetic infrastructure.
J Bioenerg Biomembr. 2015 Apr;47(1-2):1-11. doi: 10.1007/s10863-014-9570-z. Epub 2014 Aug 8.
6
Effect of high-intensity exercise on aged mouse brain mitochondria, neurogenesis, and inflammation.
Neurobiol Aging. 2014 Nov;35(11):2574-2583. doi: 10.1016/j.neurobiolaging.2014.05.033. Epub 2014 Jun 10.
7
Transcellular degradation of axonal mitochondria.
Proc Natl Acad Sci U S A. 2014 Jul 1;111(26):9633-8. doi: 10.1073/pnas.1404651111. Epub 2014 Jun 16.
8
Mitochondrial transcription factor A (Tfam) is a pro-inflammatory extracellular signaling molecule recognized by brain microglia.
Mol Cell Neurosci. 2014 May;60:88-96. doi: 10.1016/j.mcn.2014.04.003. Epub 2014 Apr 23.
9
Increased plasma levels of BDNF and inflammatory markers in Alzheimer's disease.
J Psychiatr Res. 2014 Jun;53:166-72. doi: 10.1016/j.jpsychires.2014.01.019. Epub 2014 Feb 13.
10
The Alzheimer's disease mitochondrial cascade hypothesis: progress and perspectives.
Biochim Biophys Acta. 2014 Aug;1842(8):1219-31. doi: 10.1016/j.bbadis.2013.09.010. Epub 2013 Sep 23.

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