Mitochondrial dysfunction and cellular metabolic deficiency in Alzheimer's disease

被引:32
作者
Gu, Xue-Mei [2 ]
Huang, Han-Chang [1 ,3 ]
Jiang, Zhao-Feng [1 ]
机构
[1] Beijing Union Univ, Beijing Key Lab Bioact Subst & Funct Foods, Beijing 100191, Peoples R China
[2] Beijing Mil Gen Hosp, Beijing 100700, Peoples R China
[3] Beijing Univ Chem Technol, Coll Life Sci & Technol, Beijing 100029, Peoples R China
基金
中国国家自然科学基金;
关键词
Alzheimer's disease; amyloid-beta; metabolic deficiency; mitochondrial dysfunction; AMYLOID-BETA-PEPTIDE; POSITRON-EMISSION-TOMOGRAPHY; MILD COGNITIVE IMPAIRMENT; INTRACELLULAR A-BETA; OXIDATIVE DNA-DAMAGE; GLYCERALDEHYDE-3-PHOSPHATE DEHYDROGENASE; PRECURSOR-PROTEIN; GLUCOSE-METABOLISM; ENDOPLASMIC-RETICULUM; LIPID-PEROXIDATION;
D O I
10.1007/s12264-012-1270-2
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Alzheimer's disease (AD) is an age-related neurodegenerative disorder. The pathology of AD includes amyloid-beta (A beta) 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. A beta precursor protein is cleaved to produce both extracellular and intracellular A beta, 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 A beta neurotoxicity. In this review, we summarize the pathways of A beta generation and its potential neurotoxic effects on cellular metabolism and mitochondrial dysfunction.
引用
收藏
页码:631 / 640
页数:10
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