Department of Neurodegenerative Disorders, Mossakowski Medical Research Centre, Polish Academy of Sciences, Pawińskiego 5 Str., 02-106 Warszawa, Poland.
Prog Neuropsychopharmacol Biol Psychiatry. 2011 Mar 30;35(2):320-30. doi: 10.1016/j.pnpbp.2010.07.004. Epub 2010 Jul 16.
To date, one of the most discussed hypotheses for Alzheimer's disease (AD) etiology implicates mitochondrial dysfunction and oxidative stress as one of the primary events in the course of AD. In this review we focus on the role of mitochondria and mitochondrial DNA (mtDNA) variation in AD and discuss the rationale for the involvement of mitochondrial abnormalities in AD pathology. We summarize the current data regarding the proteins involved in mitochondrial function and pathology observed in AD, and discuss the role of somatic mutations and mitochondrial haplogroups in AD development.
迄今为止，阿尔茨海默病（AD）病因学中最受关注的假说之一是线粒体功能障碍和氧化应激是 AD 病程中的主要事件之一。在这篇综述中，我们重点关注线粒体和线粒体 DNA（mtDNA）变异在 AD 中的作用，并讨论了线粒体异常参与 AD 病理的原理。我们总结了目前关于 AD 中观察到的与线粒体功能和病理学相关的蛋白质的相关数据，并讨论了体细胞突变和线粒体单倍群在 AD 发病机制中的作用。
