Milacemide therapy for Parkinson's disease

Authors

  • M. E. Giuffra,

    1. Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, U.S.A.
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  • V. H. Sethy,

    1. Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, U.S.A.
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  • T. L. Davis,

    1. Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, U.S.A.
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  • M. M. Mouradian,

    1. Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, U.S.A.
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  • Dr. T. N. Chase

    Corresponding author
    1. Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, U.S.A.
    • Building 10, Room 5C103, National Institutes of Health, Bethesda, MD 20892, U.S.A
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Abstract

The clinical effects of central glutamatergic stimulation by the glycine prodrug milacemide were studied in six patients with Parkinson's disease under double-blind, placebo-controlled conditions. When administered as monotherapy at a single oral dose of 1,200 mg, the drug increased overall parkinsonian severity transiently, mostly due to an effect on rigidity. Milacemide did not, however, alter levodopa-induced dyskinesias. These results support the view that drugs acting on the glutamatergic system can influence motor function in patients with extrapyramidal movement disorders and that pharmaceutical agents that selectively block certain subtypes of glutamate receptors may ameliorate parkinsonian symptoms.

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