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August 12, 2003; 61 (3) Article

Adenosine A2A receptor antagonist treatment of Parkinson’s disease

W. Bara-Jimenez, A. Sherzai, T. Dimitrova, A. Favit, F. Bibbiani, M. Gillespie, M.J. Morris, M.M. Mouradian, T.N. Chase
First published August 11, 2003, DOI: https://doi.org/10.1212/01.WNL.0000073136.00548.D4
W. Bara-Jimenez
From the Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD.
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A. Sherzai
From the Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD.
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T. Dimitrova
From the Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD.
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A. Favit
From the Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD.
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F. Bibbiani
From the Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD.
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M. Gillespie
From the Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD.
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M.J. Morris
From the Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD.
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M.M. Mouradian
From the Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD.
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T.N. Chase
From the Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD.
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Citation
Adenosine A2A receptor antagonist treatment of Parkinson’s disease
W. Bara-Jimenez, A. Sherzai, T. Dimitrova, A. Favit, F. Bibbiani, M. Gillespie, M.J. Morris, M.M. Mouradian, T.N. Chase
Neurology Aug 2003, 61 (3) 293-296; DOI: 10.1212/01.WNL.0000073136.00548.D4

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Abstract

Background: Observations in animal models suggest that A2A antagonists confer benefit by modulating dopaminergic effects on the striatal dysfunction associated with motor disability. This double-blind, placebo-controlled, proof-of-principle study evaluated the pathogenic contribution and therapeutic potential of adenosine A2A receptor–mediated mechanisms in Parkinson disease (PD) and levodopa-induced motor complications.

Methods: Fifteen patients with moderate to advanced PD consented to participate. All were randomized to either the selective A2A antagonist KW-6002 or matching placebo capsules in a 6-week dose-rising design (40 and 80 mg/day). Motor function was rated on the Unified PD Rating Scale.

Results: KW-6002 alone or in combination with a steady-state IV infusion of each patient’s optimal levodopa dose had no effect on parkinsonian severity. At a low dose of levodopa, however, KW-6002 (80 mg) potentiated the antiparkinsonian response by 36% (p < 0.02), but with 45% less dyskinesia compared with that induced by optimal dose levodopa alone (p < 0.05). All cardinal parkinsonian signs improved, especially resting tremor. In addition, KW-6002 prolonged the efficacy half-time of levodopa by an average of 47 minutes (76%; p < 0.05). No medically important drug toxicity occurred.

Conclusions: The results support the hypothesis that A2A receptor mechanisms contribute to symptom production in PD and that drugs able to selectively block these receptors may help palliate symptoms in levodopa-treated patients with this disorder.

  • Received October 21, 2002.
  • Accepted in final form March 22, 2003.
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