Abstract
To the Editor: γ-Aminobutyric acid (GABA) is markedly decreased in certain areas of autopsied brain from patients dying with Huntington's chorea.1 , 2 This deficiency is probably due to loss of a population of neurons that normally utilize GABA as an inhibitory neurotransmitter. Many of the symptoms of Huntington's chorea may result from crucial imbalances between GABA and other neurotransmitters, and increasing brain GABA levels might have palliative effects in the disease. Isoniazid (INH) acts as an inhibitor of GABA aminotransferase (GABA-T), the first enzyme in the degradative pathway of GABA. When given in doses higher than those used in treating tuberculosis . . .

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