Mechanisms of homocysteine neurotoxicity in neurodegenerative diseases with special reference to dementia

被引：426

作者：

Obeid, Rima ^{[1
]}

Herrmann, Wolfgang ^{[1
]}

机构：

[1] Univ Hosp Saarland, Dept Clin Chem & Lab Med, Fac Med, D-66421 Homburg, Germany

来源：

FEBS LETTERS | 2006年 / 580卷 / 13期

关键词：

homocysteine; brain; folate; vitamin B12; dementia; oxidative stress;

D O I：

10.1016/j.febslet.2006.04.088

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：

Mild to moderate hyperhomocysteinemia is a risk factor for neurodegenerative diseases. Human studies suggest that homocysteine (Hey) plays a role in brain damage, cognitive and memory decline. Numerous studies in recent years investigated the role of Hey as a cause of brain damage. Hey itself or folate and vitamin B12 deficiency can cause disturbed methylation and/or redox potentials, thus promoting calcium influx, amyloid and tau protein accumulation, apoptosis, and neuronal death. The Hey effect may also be mediated by activating the N-methyl-D-aspartate receptor subtype. Numerous neurotoxic, effects of Hey can be blocked by folate, glutamate receptor antagonists, or various antioxidants. This review describes the most important mechanisms of Hey neurotoxicity and pharmacological agents known to reverse Hey effects. (c) 2006 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

引用

页码：2994 / 3005

页数：12

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