Wilkins Heather M, Swerdlow Russell H
University of Kansas School of Medicine, MS 2012, Landon Center on Aging, 3901 Rainbow Boulevard, Kansas City, KS 66160, USA.
Curr Top Med Chem. 2016;16(8):849-57. doi: 10.2174/1568026615666150827095102.
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.
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。
