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.
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