Department of Biochemistry and Molecular Biology, Georgetown University School of Medicine, Washington, DC 20057, USA.
Mitochondrion. 2011 Jan;11(1):13-21. doi: 10.1016/j.mito.2010.08.009. Epub 2010 Sep 15.
The impairment of the respiratory chain or defects in the detoxification system can decrease electron transfer efficiency, reduce ATP production, and increase reactive oxygen species (ROS) production by mitochondria. Accumulation of ROS results in oxidative stress, a hallmark of neurodegenerative diseases such as Alzheimer's disease (AD). β-amyloid has been implicated in the pathogenesis of AD, and its accumulation may lead to degeneration of neuronal or non-neuronal cells. There is evidence that β-amyloid interacts with mitochondria but little is known concerning the significance of this interaction in the physiopathology of AD. This review explores possible mechanisms of β-amyloid-induced mitochondrial toxicity.
呼吸链的损伤或解毒系统的缺陷会降低电子传递效率，减少 ATP 的产生，并增加线粒体中活性氧（ROS）的产生。ROS 的积累会导致氧化应激，这是阿尔茨海默病（AD）等神经退行性疾病的一个标志。β-淀粉样蛋白与 AD 的发病机制有关，其积累可能导致神经元或非神经元细胞的退化。有证据表明β-淀粉样蛋白与线粒体相互作用，但对于这种相互作用在 AD 病理生理学中的意义知之甚少。这篇综述探讨了β-淀粉样蛋白诱导的线粒体毒性的可能机制。
