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Amyloid precursor protein (APP) metabolism is a key factor in the pathogenesis of Alzheimers Disease (AD) and it has been recently proposed that mitochondria are involved in the biochemical pathway by which amyloid-beta (Aβ) leads to neuronal dysfunction.The Aβ accumulated in mitochondria can decrease the level of cytochrome c oxidase Ⅳ (COX Ⅳ) and attenuate the ATP production consequently.Aβ could be produced by APP metabolism in situ or be uptaken outside of neurons.