Mitochondria, Amyloid β, and Alzheimer's Disease.
Mitochondria, Amyloid β, and Alzheimer's Disease.
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DOI：
10.4061/2011/104545
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发表时间：
2011-03-22
影响因子：
--
通讯作者：
Sullivan PG
中科院分区：
文献类型：
--
作者：
Readnower RD;Sauerbeck AD;Sullivan PG
代谢减退是阿尔茨海默病 (AD) 的一个标志，表明线粒体在与 AD 相关的神经病理学中发挥着作用。线粒体β-淀粉样蛋白 (Aβ) 积累先于细胞外 Aβ 沉积。除了增加氧化应激外，Aβ 还被证明可以直接抑制线粒体酶。氧化损伤或 Aβ 相互作用导致线粒体酶受到抑制，从而使氧化应激持续存在并导致代谢低下状态。此外，Aβ 还被证明与亲环蛋白 D 相互作用，亲环蛋白 D 是线粒体通透性转换孔的一个组成部分，可能促进细胞死亡。因此，有充分的证据表明线粒体在 AD 的病理生理学中起着至关重要的作用。
Hypometabolism is a hallmark of Alzheimer's disease (AD) and implicates a mitochondrial role in the neuropathology associated with AD. Mitochondrial amyloid-beta (Aβ) accumulation precedes extracellular Aβ deposition. In addition to increasing oxidative stress, Aβ has been shown to directly inhibit mitochondrial enzymes. Inhibition of mitochondrial enzymes as a result of oxidative damage or Aβ interaction perpetuates oxidative stress and leads to a hypometabolic state. Additionally, Aβ has also been shown to interact with cyclophilin D, a component of the mitochondrial permeability transition pore, which may promote cell death. Therefore, ample evidence exists indicating that the mitochondrion plays a vital role in the pathophysiology observed in AD.