Mitochondrial dysfunction and Alzheimer's disease

被引：99

作者：

Maruszak, Aleksandra ^{[1
]}

Zekanowski, Cezary ^{[1
]}

机构：

[1] Polish Acad Sci, Mossakowski Med Res Ctr, Dept Neurodegenerat Disorders, PL-02106 Warsaw, Poland

来源：

PROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY | 2011年 / 35卷 / 02期

关键词：

Alzheimer's disease; APOE4; Mitochondrial DNA (mtDNA); Mitochondrial dysfunction; Mitochondrial haplogroups; Oxidative stress; CYTOCHROME-C-OXIDASE; AMYLOID PRECURSOR PROTEIN; KETOGLUTARATE DEHYDROGENASE COMPLEX; OXIDATIVELY MODIFIED PROTEINS; MILD COGNITIVE IMPAIRMENT; APOLIPOPROTEIN-E GENOTYPE; OXYGEN SPECIES PRODUCTION; MATERNAL FAMILY-HISTORY; FREE-RADICAL GENERATION; MTDNA CONTROL-REGION;

D O I：

10.1016/j.pnpbp.2010.07.004

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

To date, one of the most discussed hypotheses for Alzheimer's disease (AD) etiology implicates mitochondrial dysfunction and oxidative stress as one of the primary events in the course of AD. In this review we focus on the role of mitochondria and mitochondrial DNA (mtDNA) variation in AD and discuss the rationale for the involvement of mitochondrial abnormalities in AD pathology. We summarize the current data regarding the proteins involved in mitochondrial function and pathology observed in AD, and discuss the role of somatic mutations and mitochondrial haplogroups in AD development. (C) 2010 Elsevier Inc. All rights reserved.

引用

页码：320 / 330

页数：11

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