The research involved 136,474 people who did not have Parkinson’s disease at the beginning of the research. Participants were asked about their use of non-steroid anti-inflammatory drugs (NSAIDs), including aspirin, ibuprofen and acetaminophen. After six years, 293 participants had developed Parkinson’s disease.

The study found regular users of ibuprofen were 40 percent less likely to develop Parkinson’s disease than people who didn’t take ibuprofen. Also, people who took higher amounts of ibuprofen were less likely to develop Parkinson’s disease than people who took smaller amounts of the drug. The results were the same regardless of age, smoking and caffeine intake.

"Ibuprofen was the only NSAID linked to a lower risk of Parkinson’s," said Xiang Gao, MD, with Harvard School of Public Health in Boston. "Other NSAIDs and analgesics, including aspirin and acetaminophen, did not appear to have any effect on lowering a person’s risk of developing Parkinson’s. More research is needed as to how and why ibuprofen appears to reduce the risk of Parkinson’s disease, which affects up to one million people in the United States."

Abstracted from Science Daily, Febuary 18, 2010

We were interested in Parkinson’s disease becasue it is the second most common neurodegenerative disorder in the Western world, and a major cause of disability and distress among older Americans. Family studies have long indicated that Parkinson’s is a genetic disorder when certain mutations are inherited. However, specific genetic factors relevant to the general population have been elusive.

The PD gene that we investigated is called leucine risk repeat kinase 2 (LRRK2) which encodes a protein called dardarin, derived from the Basque word dardara, meaning tremor. Mutations in LRRK2 are a common cause of familial Parkinson’s disease. This study published in the Annals of Human Genetics describes a combination of four gene variants found in a third of Parkinson’s cases, but infrequent in the population. Thus the presence or absence of this signature can be used as a genetic test for Parkinson’s disease. [Patent pending]

Earlier work had identified each of the four variants as being associated with PD risk, but did not combine the information to make a specific risk signature.

Genetic testing using this approach is expected to identify a third of persons at very high risk. It will not identify other genetic factors or level of risk due to environmental exposures, such as pesticides, and lifestyle. Thus the absence of this risk signature does not guarantee low risk. This finding helps us understand what causes PD and could lead to new and more effective avenues for prevention and treatment. The advance is expected to identify individuals at greatest risk for PD before symptoms arise, when therapies and lifestyle changes might be most effective in slowing disease progression.

In 1993, I was the lead author on the Science article that described how risk for Alzheimer’s disease multiplied according to the number of copies of the apolipoprotein E allele 4 inherited from parents. This finding has been replicated in hundreds of studies and remains the one established genetic risk factor for Alzheimer’s disease, and the prototype for investigating common gene variants for common disorders. We continue to investigate the genetic underpinnings of PD.