Abstract
Recent identification of glutamate as a transmitter in neocortical efferents and discovery of toxic effects of excessive amounts of extra-cellular glutamate or its analogues on some brain neurons offer an explanation of the pathogenesis of Huntington's chorea. Cell death as well as consequent biochemical changes and clinical symptoms in this disease possibly result from excessive excitation of the neostriatal, and of some other neurons by glutamate released from neocortical axon terminals. If so, the development of Huntington's chorea could be prevented or arrested by blockers of glutamate transmissions, and folate should be reduced to the minimum in the diet of the genetically marked families.
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