Folate and homocysteine metabolism in neural plasticity and neurodegenerative disorders

被引:740
作者
Mattson, MP
Shea, TB
机构
[1] NIA, Gerontol Res Ctr, Neurosci Lab, Baltimore, MD 21224 USA
[2] Univ Massachusetts, Dept Biol Sci, Ctr Cellular Neurobiol & Neurodegenerat Res, Lowell, MA 01854 USA
关键词
BETA-SYNTHASE DEFICIENCY; FOLIC-ACID; METHYLENETETRAHYDROFOLATE-REDUCTASE; PLASMA HOMOCYSTEINE; APOLIPOPROTEIN-E; S-ADENOSYLMETHIONINE; RISK-FACTOR; 5,10-METHYLENETETRAHYDROFOLATE REDUCTASE; VITAMIN-B-12; DEFICIENCY; COMBINED DEGENERATION;
D O I
10.1016/S0166-2236(03)00032-8
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Folate is a cofactor in one-carbon metabolism, during which it promotes the remethylation of homocysteine-a cytotoxic sulfur-containing amino acid that can induce DNA strand breakage, oxidative stress and apoptosis. Dietary folate is required for normal development of the nervous system, playing important roles regulating neurogenesis and programmed cell death. Recent epidemiological and experimental studies have linked folate deficiency and resultant increased homocysteine levels with several neurodegenerative conditions, including stroke, Alzheimer's disease and Parkinson's disease. Moreover, genetic and clinical data suggest roles for folate and homocysteine in the pathogenesis of psychiatric disorders. A better understanding of the roles of folate and homocysteine in neuronal homeostasis throughout life is revealing novel approaches for preventing and treating neurological disorders.
引用
收藏
页码:137 / 146
页数:10
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