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Mitochondrial dysfunction and cellular metabolic deficiency in Alzheimer’s disease

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Abstract

Alzheimer’s disease (AD) is an age-related neurodegenerative disorder. The pathology of AD includes amyloid-β (Aβ) deposits in neuritic plaques and neurofibrillary tangles composed of hyperphosphorylated tau, as well as neuronal loss in specific brain regions. Increasing epidemiological and functional neuroimaging evidence indicates that global and regional disruptions in brain metabolism are involved in the pathogenesis of this disease. Aβ precursor protein is cleaved to produce both extracellular and intracellular Aβ, accumulation of which might interfere with the homeostasis of cellular metabolism. Mitochondria are highly dynamic organelles that not only supply the main energy to the cell but also regulate apoptosis. Mitochondrial dysfunction might contribute to Aβ neurotoxicity. In this review, we summarize the pathways of Aβ generation and its potential neurotoxic effects on cellular metabolism and mitochondrial dysfunction.

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  1. Beijing Military General Hospital, Beijing, 100700, China

    Xue-Mei Gu

  2. Beijing Key Laboratory of Bioactive Substances and Functional Foods, Beijing Union University, Beijing, 100191, China

    Han-Chang Huang & Zhao-Feng Jiang

  3. College of Life Science and Technology, Beijing University of Chemical Technology, Beijing, 100029, China

    Han-Chang Huang

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Gu, XM., Huang, HC. & Jiang, ZF. Mitochondrial dysfunction and cellular metabolic deficiency in Alzheimer’s disease. Neurosci. Bull. 28, 631–640 (2012). https://doi.org/10.1007/s12264-012-1270-2

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