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Neuroprotection by caffeine and more specific A_2A receptor antagonists in animal models of Parkinson’s disease

From the Department of Neurology (Drs. Schwarzschild, Xu, and Chen), Massachusetts General Hospital, Boston, MA; Department of Chemistry (Drs. Petzer and Castagnoli, K. Castagnoli), Virginia Polytechnic Institute and State University, Blacksburg, VA; and Department of Neurology (Drs. Oztas and Chen), Boston University School of Medicine, Boston, MA.

Address correspondence and reprint requests to Dr. Michael A. Schwarzschild, Center for Aging, Genetics and Neurodegeneration, Massachusetts General Hospital, 114 16th Street, Boston, MA 02129; e-mail: michaels{at}helix.mgh.harvard.edu

A remarkable convergence of epidemiologic and laboratory data has raised the possibility that caffeine reduces the risk of developing Parkinson’s disease (PD) by preventing the degeneration of nigrostriatal dopaminergic neurons. The authors review the evidence that caffeine and more specific antagonists of the adenosine A_2A receptor protect dopaminergic neurons in several toxin models of PD. Other studies demonstrating protection by A_2A receptor inactivation in animal models of stroke, Huntington’s disease, and Alzheimer’s disease suggest a more global role of A_2A receptors in neuronal injury and degeneration. Although the cellular and molecular mechanisms by which A_2A receptors contribute to neuronal death are not yet established, several intriguing possibilities have emerged. Now with preliminary clinical data substantiating the antiparkinsonian symptomatic benefit of A_2A receptor blockade, the prospects for a complementary neuroprotective benefit have enhanced the therapeutic potential of A_2A antagonists in PD.

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