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兴奋性氨基酸、自由基与运动神经元病的发病机制。

Excitatory amino acids, free radicals and the pathogenesis of motor neuron disease.

作者信息

Zeman S, Lloyd C, Meldrum B, Leigh P N

机构信息

Department of Neurology, Institute of Psychiatry, London, UK.

出版信息

Neuropathol Appl Neurobiol. 1994 Jun;20(3):219-31. doi: 10.1111/j.1365-2990.1994.tb00963.x.

DOI:10.1111/j.1365-2990.1994.tb00963.x
PMID:7936071
Abstract

The cause of motor neuron disease (MND) remains unknown, but the pathogenic involvement of excitatory amino acid (EAA) neurotransmitters and related exogenous compounds has been proposed. We discuss current concepts of the mechanisms of action of EAAs and the evidence for links between these neurotransmitters and free radical hypotheses of neuronal damage. These concepts are especially pertinent following reports of mutations in the gene encoding the free radical scavenging enzyme, copper-zinc superoxide dismutase, in familial MND. New approaches to treatment are suggested by advances in understanding of the disease.

摘要

运动神经元病(MND)的病因尚不清楚,但已有研究提出兴奋性氨基酸(EAA)神经递质及相关外源性化合物参与了其发病机制。我们将探讨EAA作用机制的当前概念,以及这些神经递质与神经元损伤自由基假说之间联系的证据。在家族性MND中,编码自由基清除酶铜锌超氧化物歧化酶的基因突变报告出现后,这些概念尤为相关。对该疾病认识的进展为新的治疗方法提供了思路。

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