Caffeine and the Risks of Disease Progression and Dyskinesias in PD
Fast Track, 2001
A remarkable convergence of recent epidemiological and laboratory data has raised the possibility that dietary caffeine may reduce the risk of developing Parkinson's disease (PD). In our animal studies we have found that caffeine (and more specific antagonists of the A2A adenosine receptor) can reduce dopaminergic neurotoxicity in the MPTP model of PD. In addition, we and others have found that genetic or pharmacological inactivation of the A2A receptor may prevent excessive motor responses to repeated L-dopa treatment in an animal model of the dyskinesias, which are a major complication of L-dopa therapy in PD. Together these data have led us to hypothesize that caffeine consumption is inversely and dose-dependently associated with (1) disease progression in PD, and (2) the development of dyskinesias and other dopaminergic motor complications in PD. We propose to test this hypothesis in an extremely well-characterized cohort of PD patients (CALM-PD study subjects) whose disease progression and dopaminergic motor complications have been rigorously documented by complementary clinical scales and functional neuroimaging studies. A caffeine questionnaire will be administered to these patients, and then rates of caffeine consumption will be correlated with rates of disease progression (UPDRS and b-CIT) and dyskinesia development. The results may provide important clues to the pathophysiology, epidemiology and therapy of PD.
Professor of Neurology at Harvard Medical School
Director, Molecular Neurobiology Laboratory at Massachusetts General Hospital
Location: Boston, Massachusetts