Long term treatment of Huntington disease with L‐glutamate and pyridoxine

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Abstract
Decreased levels of .gamma.-aminobutyric acid (GABA) and its synthetic enzyme, glutamic acid decarboxylase, were found in the brains of patients with Huntington disease. In an attempt to augment GABA-mediated neurotransmission, daily doses of 25 g of L-glutamate (the substrate for glutamic acid decarboxylase) and 500 mg of pyridoxine, its cofactor, were given to 5 patients with Huntington disease. This regimen was continued for 2 yr. Assessment of motor and behavioral function indicated no improvement on this regimen.

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