Those with highest amount had almost half the risk of needing to start treatment
MONDAY, April 14 (HealthDay News) -- Men with naturally high levels of the antioxidant urate in their blood appear to develop the symptoms of Parkinson's disease slower than those with lower levels do, a new report says.
The findings, published in the April issue of the Archives of Neurology, support early laboratory studies about urate's protective qualities and offer hope for future disease therapies to delay Parkinson's symptoms such as tremors, rigidity and difficulty walking and talking.
Urate is a salt derived from uric acid, and it is a normal component of blood; however, high levels can lead to gout and kidney stones.
In a two-year study of 800 men recently diagnosed with Parkinson's, researchers from the MassGeneral Institute for Neurodegenerative Disease and Harvard School of Public Health found that those with the highest urate levels at the study's start had almost half the risk of needing to start Parkinson's treatment drugs as did those with the lowest levels.
Brain scans showed that participants with higher urate levels also lost the fewest dopamine-producing neurons. Parkinson's disease is caused when brain cells that produce the neurotransmitter dopamine are destroyed.
"These findings, combined with prior knowledge of urate's protective properties in laboratory studies, raise the possibility that urate-elevating strategies could be used to slow the neurodegeneration of Parkinson's disease," study author Michael Schwarzschild, an associate professor of neurology at Harvard Medical School, said in a prepared statement.
"Potential benefits of urate have to be tempered against the known risks of elevated urate levels, which include gout and kidney stones. From what we know now, urate elevation should only be attempted in the context of a closely monitored clinical trial, in which potential benefits and risks are carefully balanced," Schwarzschild said.
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SOURCE: Harvard School of Public Health/Massachusetts General Hospital, news release, April 14, 2008
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