兴奋毒性
谷氨酸受体
兴奋性氨基酸转运体
谷氨酸的
冲程(发动机)
缺血
神经科学
缺血性中风
医学
内科学
生物
受体
机械工程
工程类
出处
期刊:Int J Cerebrovasc Dis
日期:2013-02-15
卷期号:21 (02): 132-137
标识
DOI:10.3760/cma.j.issn.1673-4165.2013.02.011
摘要
The mechanisms underlying early neurological deterioration (END) after ischemic stroke are not clear. There are no reliable predictive factors and effective preventive measures for END. The glutamate-mediated excitotoxicity plays a very important role in the cascade reaction of ischemic events. High level of glutamate in plasma is one of the important predictors for END. Studies have shown that the polymorphism in the promoter of the excitatory amino acid transporter-2 gene is a potential cause for individual susceptibility to END. Some therapeutic strategies of interrupting the glutamatergic pathways may be as the strategies of intervention END.
Key words:
Stroke; Brain Ischemia; Glutamic Acid; Biological Markers; Disease Progression
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