No such relationships were seen for aspirin, acetaminophen, or NSAIDs other than ibuprofen grouped together. Roughly as many participants reported taking these agents as they did ibuprofen.
When the analysis was expanded to include findings from six other prospective studies, including 2,779 Parkinson cases, with data on NSAID use, ibuprofen was still associated with lower disease risk, whereas other drugs were not.
The relative risk for Parkinson's disease in the pooled data was a 27 percent reduction, Gao and colleagues reported.
They noted that, unlike other NSAIDs and acetaminophen, ibuprofen is an agonist at PPAR-gamma receptors.
Dr. David Standaert, interim chairman of neurology at the University of Alabama at Birmingham, told MedPage Today and ABC News that the findings and the presumed mechanism were both plausible.
He said his own research had suggested that, while Parkinson's disease is probably triggered by a variety of factors, inflammation in the brain is what drives it along. "A simple way to express this is to say that inflammation does not start the fire, but it is responsible for keeping it burning," he said in an email.
But, he added, "the PPAR-gamma mechanism is a reasonable concept as well."
Another class of medications also targets PPAR-gamma -- the glitazone drugs used to treat type 2 diabetes.
A clinical trial based at the University of Rochester is now gearing up to test the PPAR-gamma theory of Parkinson's disease. Patients with early-stage disease will take pioglitazone (Actos) or placebo for 44 weeks. The trial's primary outcome measure will be disease progression according to the UPDRS rating scale.
In their editorial, Bower and Ritz agreed that the mechanism deserved a clinical trial -- and ideally with "a safer PPAR-gamma agonist" than ibuprofen.