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MIAMI BEACH—A study of non-steroidal inflammatory drugs (NSAIDs) in 147,000 people found that ibuprofen, but not other NSAIDs, appeared to prevent or delay Parkinson disease (PD). Alberto Ascherio, MD, DrPH, Associate Professor of Nutrition and Epidemiology at the Harvard School of Public Health, and co-investigator Honglei Chen, MD, PhD, presented the results of the current study here at the AAN Annual Meeting in April.

It was the second large-scale study by the same group at the Harvard School of Public Health to suggest that non-NSAIDs have some protective effect in PD. But it was the first to conclude that ibuprofen (Motrin), but not the other NSAIDS, have this effect.

The study was based on data drawn from the American Cancer Society's Cancer Prevention Study II Nutrition Cohort, in which participants were recruited from 1992 to 2000.

The participants were asked about their use of ibuprofen and other non-aspirin NSAIDs in 1992 and 1997. The incident PD cases were identified by a self-report followed by confirmation by the treating neurologists or by review of the medical records. The results were adjusted for age, sex, smoking, and other potential confounders. Researchers identified 413 PD cases that developed in the course of their study.


The key result: participants who answered that they took two or more tablets of ibuprofen a week in the previous year or longer had a 35 percent reduced risk of developing the disease compared with those not regularly taking the drug. Participants who took the drug daily had a 38 percent reduced risk as compared to nonusers, said Dr. Ascherio, who is also Associate Professor of Medicine at Harvard Medical School.

The researchers also found no significant associations between use of aspirin, other NSAIDs, and risk of PD.

The results were similar in men and women. At the time of recruitment, they were between 40 to 79 years, with a mean age of 62.

“The real strength of the study is that all the information was collected before the onset of Parkinson disease,” ensuring a more accurate accounting of their drugs, Dr. Ascherio said.


“Our study suggests that ibuprofen may have effects different from other COX inhibitors,” he said. “This concept, which is supported by similar findings in previous studies of Alzheimer disease, has important implications for future studies on potential benefits of NSAIDs in neurodegenerative diseases.”

Joseph Jankovic, MD, Professor of Neurology and Director of the Parkinson's Disease Center and Movement Disorders Clinic at Baylor College of Medicine, said the report was “quite intriguing in that it supports the growing evidence that glial-cell-mediated inflammatory events play a role in the pathogenesis of PD.”

Dr. Jankovic also noted that the study is in part consistent with another study published by the same group in 2003. In that study, they used the Health Professional Follow-up Study to prospectively investigate whether the use of NSAIDs delays the onset of or prevents PD (Arch Neurol 2003;60:1059–1064).

He said the finding of a protective benefit of NSAIDs in that study, while statistically significant, was not robust. “Ninety-eight individuals would have to be treated with NSAIDs for 10 years to prevent one case of PD,” Dr. Jankovic said.

“The current study does not address the question why ibuprofen, but not other NSAIDs, lowered the risk of PD,” he said, adding to that is growing concern about potential vascular risks of NSAIDs. “Therefore,” he added, “I think that it is premature to recommend ibuprofen as a prophylactic drug against PD. Further studies, of course, are needed to explore the unique properties of ibuprofen as compared to the other NSAIDs.”

“Could the drug work through other mechanisms, similar, for example, to those of minocycline and other tetracycline derivatives?” he wondered. They also have been implicated as potential neuroprotective agents, acting possibly not only as anti-inflammatory drugs, but also as anti-apoptotic agents.


Cynthia L. Comella, MD, Associate Professor in the Department of Neurological Sciences at Rush University Medical Center, said, “This study is interesting but still preliminary.” She noted earlier studies in animal models that indicated that anti-inflammatory drugs might preserve dopamine neuronal integrity.

“Taken together, these studies seem to suggest that inflammation may play some role in the development of PD.” She said, though, that further studies would have to confirm this hypothesis and define the usefulness of these drugs in PD.

And anti-inflammatory drugs are not the only substance associated with a protective effect in Parkinson disease. In 2001, Dr. Ascherio and his colleagues reported (Ann Neurology 2001; 50:56–63) moderate amounts of caffeine could also cut their risk of PD by up to half. That was based on a study involving more than 130,000 participants in two ongoing cohorts, the Health Professionals' Follow-Up Study and the Nurses' Health Study.

G. Webster Ross, MD, of the Department of Veterans Affairs in Honolulu, and colleagues also reported a protective effect of caffeine one year earlier (JAMA 2000;283:2674–2679), after 30 years of follow-up of 8,004 Japanese-American men in the Honolulu Heart Program.


  • ✓ An analysis of data drawn from the American Cancer Society's Cancer Prevention Study II Nutrition Cohort showed that participants who took ibuprofen daily had a 38 percent reduced risk for Parkinson disease as compared to nonusers.


• Chen H, Zhang SM, Ascherio A, et al. Nonsteroidal anti-inflammatory drugs and the risk of Parkinson disease. Arch Neurol 2003;60:1059–1064.