神经毒性
高同型半胱氨酸血症
同型半胱氨酸
谷氨酸受体
痴呆
NMDA受体
兴奋毒性
神经保护
认知功能衰退
受体
医学
药理学
神经科学
内科学
生物
毒性
疾病
作者
Rima Obeid,Wolfgang Herrmann
出处
期刊:FEBS Letters
[Wiley]
日期:2006-05-06
卷期号:580 (13): 2994-3005
被引量:420
标识
DOI:10.1016/j.febslet.2006.04.088
摘要
Mild to moderate hyperhomocysteinemia is a risk factor for neurodegenerative diseases. Human studies suggest that homocysteine (Hcy) plays a role in brain damage, cognitive and memory decline. Numerous studies in recent years investigated the role of Hcy as a cause of brain damage. Hcy 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 Hcy effect may also be mediated by activating the N ‐methyl‐ d ‐aspartate receptor subtype. Numerous neurotoxic effects of Hcy can be blocked by folate, glutamate receptor antagonists, or various antioxidants. This review describes the most important mechanisms of Hcy neurotoxicity and pharmacological agents known to reverse Hcy effects.
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