Glutamate dysfunction and selective motor neuron degeneration in amyotrophic lateral sclerosis: a hypothesis.
Glutamate dysfunction and selective motor neuron degeneration in amyotrophic lateral sclerosis: a hypothesis.
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肌萎缩侧索硬化症中的谷氨酸功能障碍和选择性运动神经元变性：一种假设。
DOI：
10.1002/ana.410280103
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发表时间：
1990
影响因子：
11.2
通讯作者：
Plaitakis,A
中科院分区：
文献类型：
--
作者：
Plaitakis,A
最近的研究表明，肌萎缩侧索硬化症患者谷氨酸代谢普遍存在缺陷，这与中枢神经系统中这种兴奋性氨基酸被认为是递质的水平的广泛改变有关。目前的数据支持这样的假设，即突触前谷氨酸能机制的改变可能是导致这种疾病中神经兴奋毒性细胞损失的原因。从甘氨酸末端释放的高浓度局部甘氨酸可能破坏适应性过程，导致谷氨酸受体介导的兴奋性传递异常增强，并导致运动神经元的选择性变性。这些考虑为肌萎缩性侧索硬化症提供了新的治疗策略。
Recent studies provided evidence for a generalized defect in glutamate metabolism in patients with amyotrophic lateral sclerosis, associated with widespread alterations in the central nervous system levels of this excitatory amino acid putative transmitter. Present data support the hypothesis that altered presynaptic glutamatergic mechanisms may be responsible for a neuroexcitotoxic cell loss in this disorder. High local concentrations of glycine, released from glycinergic terminals, may disrupt adaptive processes contributing to abnormal potentiation of excitatory transmission mediated by glutamate receptors and resultant selective degeneration of motor neurons. These considerations offer new therapeutic strategies for amyotrophic lateral sclerosis.