The Role of Mitochondrial Dysfunction in the Progression of Alzheimer's Disease

被引：51

作者：

Desler, Claus ^{[1
]}

Lillenes, Meryl S. ^{[2
]}

Tonjum, Tone ^{[2
]}

Rasmussen, Lene Juel ^{[1
]}

机构：

[1] Univ Copenhagen, Dept Cellular & Mol Med, Ctr Hlth Aging, Copenhagen, Denmark

[2] Oslo Univ Hosp, Dept Microbiol, HBAC, Oslo, Norway

来源：

CURRENT MEDICINAL CHEMISTRY | 2018年 / 25卷 / 40期

关键词：

Mitochondria; DNA repair; dNTP pools; nucleotide metabolism; brain; BASE EXCISION-REPAIR; MAMMALIAN RIBONUCLEOTIDE REDUCTASE; MEMBRANE PHOSPHOLIPID ALTERATIONS; 8-OXOGUANINE DNA GLYCOSYLASE; DE-NOVO SYNTHESIS; OXIDATIVE DAMAGE; GLUTATHIONE-PEROXIDASE; NADPH OXIDASE; AMYLOID-BETA; DIHYDROOROTATE DEHYDROGENASE;

D O I：

10.2174/0929867324666170616110111

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The current molecular understanding of Alzheimer's disease (AD) has still not resulted in successful interventions. Mitochondrial dysfunction of the AD brain is currently emerging as a hallmark of this disease. One mitochondrial function often affected in AD is oxidative phosphorylation responsible for ATP production, but also for production of reactive oxygen species (ROS) and for the de novo synthesis of pyrimidines. This paper reviews the role of mitochondrial produced ROS and pyrimidines in the aetiology of AD and their proposed role in oxidative degeneration of macromolecules, synthesis of essential phospholipids and maintenance of mitochondrial viability in the AD brain.

引用

页码：5578 / 5587

页数：10

共 123 条

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