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Exercise Protects Against Parkinson's
Thursday October 22, 2009
Society for Neuroscience - Long-term exercise protects against the loss of dopamine-producing cells and energy-producing mitochondria in neurons, which are important for maintaining function and movement in a chronic mouse model of Parkinson's disease, a new study reports.
These results, report at the Neuroscience 2009 Show in Chicago, support the concept that exercise may slow the progression of Parkinson's disease.
"Clinical reports have implicated exercise training in improving the physical performance and mobility of people with Parkinson's disease, but no one has demonstrated, either clinically or in laboratory models, whether exercise can delay the progression of neuronal degeneration," says senior author Yuen-Sum Lau at the Univ. of Houston. "This study was aimed at investigating this possibility and at examining how exercise protects neural mitochondria."
In people with Parkinson's disease, mitochondria-the energy factory of cells-become sluggish, which contributes to the death of dopamine neurons in brain areas that control motor functions. The loss of dopamine neurons is believed to trigger the symptoms of Parkinson's disease.
The mice used in the study were chronically induced with a neurotoxin to have many features that resemble human Parkinson's disease, including impaired movement and a marked loss of brain dopamine and mitochondrial function. The animals were divided into two groups: one was kept sedentary; the other exercised on a motorized treadmill for 40 minutes daily, five days a week, for 18 weeks. At the end of the study, the exercise-trained Parkinson's mice had significantly higher brain dopamine content and exhibited greater brain mitochondrial activity than the sedentary mice. They also performed better in a test that assessed their balancing abilities.
"This research provides scientific evidence that long-term endurance exercise protects brain mitochondria and dopamine-producing neurons from undergoing progressive degeneration as demonstrated in the chronic mice model of Parkinson's disease," says Lau.
Their research was supported by the NIH's National Institute of Neurological Diseases and Stroke.
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