Rethinking Alzheimer's Disease Therapy: Are Mitochondria the Key?

被引：43

作者：

Ankarcrona, Maria ^{[1
]}

Mangialasche, Francesca ^{[2
,3
]}

Winblad, Bengt ^{[1
]}

机构：

[1] Karolinska Inst, KI Alzheimers Dis Res Ctr, Dept Neurobiol, Care Sci & Soc NVS, SE-14186 Huddinge, Sweden

[2] Karolinska Inst, Aging Res Ctr, Stockholm, Sweden

[3] Univ Perugia, Inst Gerontol & Geriatr, Dept Clin & Expt Med, I-06100 Perugia, Italy

来源：

JOURNAL OF ALZHEIMERS DISEASE | 2010年 / 20卷

关键词：

Alzheimer's disease; drug target; mitochondria; therapy; DEHYDROGENASE COMPLEX ACTIVITY; MILD COGNITIVE IMPAIRMENT; CYTOCHROME-C-OXIDASE; A-BETA; VITAMIN-E; GAMMA-SECRETASE; GLUCOSE-TRANSPORTER; PRECURSOR PROTEIN; OXIDATIVE STRESS; TRANSGENIC MICE;

D O I：

10.3233/JAD-2010-100327

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

The number of people suffering from Alzheimer's disease (AD) is constantly increasing worldwide since humans live longer and age is the strongest risk factor for AD. Currently available medications for AD do not interfere with the progressive loss of synapses and neurons in the All brain. Therefore, the development of disease modifying therapies is a major future goal. Mitochondria provide cellular energy and are crucial for proper neuronal activity and survival. Mitochondrial dysfunction is evident in early stages of AD and is involved in AD pathogenesis. The development of drugs that protect mitochondria from damage is therefore a promising strategy for AD therapy. In this review, we will discuss current available medications for AD, drugs under clinical testing, and mitochondria as a novel drug target.

引用

页码：S579 / S590

页数：12

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