文献类型：期刊文献

英文题名：Mitochondrial dysfunction and cellular metabolic deficiency in Alzheimer's disease

作者：Gu, Xue-Mei[2];Huang, Han-Chang[1,3];Jiang, Zhao-Feng[1]

第一作者：Gu, Xue-Mei

通讯作者：Jiang, ZF[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

第一机构：北京联合大学生物化学工程学院|北京联合大学应用文理学院

通讯机构：[1]corresponding author), Beijing Union Univ, Beijing Key Lab Bioact Subst & Funct Foods, Beijing 100191, Peoples R China.|[1141726]北京联合大学生物化学工程学院;[11417]北京联合大学;[114172]北京联合大学应用文理学院;

年份：2012

卷号：28

期号：5

起止页码：631-640

外文期刊名：NEUROSCIENCE BULLETIN

收录：;Scopus(收录号：2-s2.0-84871452231);WOS:【SCI-EXPANDED(收录号:WOS:000309357800019)】；

基金：This review was supported by the National Natural Science Foundation of China (31071512), the Subsidy for Outstanding People of Beijing Municipality, China (2012D005022000006) and the Project for Academic Human Resources Development in Institutions of Higher Learning Under the Jurisdiction of Beijing Municipality, China [PHR(IHLB), PHR20090514].

语种：英文

外文关键词：Alzheimer's disease; amyloid-beta; metabolic deficiency; mitochondrial dysfunction

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.