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Exercise Helps Slow Parkinson's Disease

Regular Exercise Triggers Important Brain-Preserving Proteins
WebMD Health News

Oct. 25, 2004 -- Exercise may slow the onset of Parkinson's disease, a new animal study shows. A pilot study is under way to test this theory in Parkinson's disease patients.

It's a wake-up call for the rest of us to get some regular exercise, the researchers say.

"The concept is emerging that exercise is not only good for the heart and body weight, but also good for the brain," senior researcher Michael J. Zigmond, PhD, co-director of the Center for Neurosciences at the University of Pittsburgh School of Medicine, tells WebMD.

Zigmond heads the team presenting this newest report at the Society for Neuroscience annual meeting, held in San Diego this week.

"Studies show consistently that people who lead active lives -- who exercise and walk every day -- are less likely to get Parkinson's disease," Zigmond says. "Studies are also under way to identify individuals with Parkinson's disease, put them on an exercise regimen, to see if it is preventive. In the next few years, we should have a real handle on that."

Parkinson's disease is a mystery, its cause unknown but the symptoms unmistakable. The progression of this brain-wasting disease causes uncontrollable tremors, rigidity of limbs, slow movements, and stooped posture. This results from the slow breakdown of nerve cells in the brain that produce dopamine, a chemical that helps control movement.

While some medications or surgery help relieve symptoms, researchers have searched for ways to prevent the downward spiral of Parkinson's disease. This newest study offers hope for an extremely doable alternative, says Zigmond.

Simulating Parkinson's Disease

In their study, the Pittsburgh researchers first put a cast on a lab rat's forearm and forced the rat to exercise the other "good arm" for seven days. Researchers then removed the cast, and -- to simulate Parkinson's disease -- injected one side of the rat's brain (the same side as the casted limb) with a toxin that triggers brain cell loss, mimicking what is seen in Parkinson's disease.

The side of the brain that was injected was chosen because it controls movement in the free limb. By casting the opposite limb, the researchers were hoping to force exercise in the limb that should have had its movement destroyed by the brain toxin.

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