Experts at Massachusetts General Hospital have found in a study that higher blood levels of a compound called urate is associated with a slower progression of Parkinson's disease.
Writing about their findings in an article, posted in the online journal Archives of Neurology, the researchers revealed that urate is a salt derived from uric acid that is associated with gout.
The article also suggests that urate is a powerful antioxidant that circulates at high levels in the human bloodstream.
Its authors write that urate may prevent cells from being damaged by nitrogen and oxygen in a process scientifically known as oxidative stress.
Their observation holds significance for the prevention of Parkinson's disease, which may due to the loss of brain cells that produce dopamine as a result of oxidative stress.
During the study, 804 individuals with early Parkinson's disease were studied. All the participants were persons who were enrolled in a drug trial conducted between April 2002 and August 2005.
Led by Dr. Michael A. Schwarzschild, a team of researchers measured blood urate levels of the participants at the beginning of the study.
The subjects were then seen one month later, and again every three months until 24 months had passed.
Each time, the subjects were assessed to determine whether their disease had progressed enough to require dopaminergic therapy.
By the end of the study, 493 participants (61 percent) became disabled enough by their Parkinson's disease to require dopaminergic therapy.
The researchers noted that patients having high blood urate levels were less likely to progress to that point.
The subjects were then divided into five groups on the basis of their blood levels of urate.
Upon further study on those groups, the researchers observed that people in the group with the highest levels were half as likely to require dopaminergic therapy, compared to those with the lowest levels.
The authors of the study write that the apparent association between urate levels and Parkinson's disease progression may indicate that urate itself protects dopamine-producing neurons that are typically destroyed as the condition worsens, and that, alternatively, other compounds that the body eventually turns into urate may be neuroprotective.
"Measurement of urate on its own in patients with newly diagnosed Parkinson's disease as an indicator of an individual patient's future rate of progression is likely to be of modest clinical utility," the authors write.
However, targeting urate or its precursors could be a promising pathway for the development of therapies to treat Parkinson's disease.