Boosting Protein Output Shields Against Parkinson's: Study

by VR Sreeraman on  February 3, 2009 at 2:04 PM Research News
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Boosting the output of a protein produced by brain cells called astrocytes can provide complete protection from Parkinson's disease, a study published Monday showed.
 Boosting Protein Output Shields Against Parkinson's: Study
Boosting Protein Output Shields Against Parkinson's: Study

A movement disorder characterized by tremors and sluggishness, Parkinson's disease occurs when dopamine-producing nerve cells in a part of the brain called the substantia nigra die or become impaired, making the body's muscles less able to function smoothly and in a coordinated manner.

Boxer Muhammad Ali, actor Michael J. Fox and the late pope John Paul II are among well-known sufferers of the disease.

In the study, the results of which were published in the Proceedings of the National Academy of Sciences, researchers at the University of Wisconsin-Madison studied mice with astrocytes that produced twice the normal level of a protein called Nrf2.

Even when the mice were pumped full of a chemical known to cause Parkinson's disease they were completely protected from the movement disorder, the study showed, concluding that it was the Nrf2 protein produced by the astrocytes which shielded the mice from the chemical's toxic effects.

Pei-Chun Chen, a postdoctoral fellow from Taiwan, crossed the mouse that over-produced Nrf2 with another mouse in which the protein was "knocked out," and found that the "knock-out" mouse was also completely protected from the chemical toxicity which causes Parkinson's disease.

"The dopamine metabolite level was reduced by 90 percent in the knock-out mouse, but it was completely untouched with Nrf2 in astrocytes" and did not develop Parkinson's, said Jeffrey Johnson, a professor in pharmaceutical sciences at the University of Wisconsin who led the study.

"We didn't expect the complete abolition of toxicity," Johnson told AFP.

In December, University of Wisconsin scientists found that increasing Nrf2 could delay the onset of amyotrophic lateral sclerosis, or Lou Gehrig's disease, and studies are ongoing to determine the effect of the protein on sufferers of the neuro-degenerative Alzheimer's and Huntington's diseases.

"My instinct is that astrocyte dysfunction is probably common to all these diseases," Johnson said.

"It's becoming apparent that astrocyte dysfunction is a major contributing factor to the neurons dying," Johnson said.

"If we can make the astrocyte better or stronger, or so that it doesn't become dysfunctional, you can preserve the neurons," he said.

The researchers have begun long-term experiments in mice to see if intervention to reverse Parkinson's is possible after damage has already occurred.

"Parkinson's disease patients, by the time they are diagnosed, there's a significant loss of neural function," said Johnson.

"The question is: how many of those neurons are actually dead or just not working right?

"If neurons are still there but can't function because of the environment, changing the environment may not only prevent further loss, but it may also make those that are sick healthy again, and you may get cell recovery," Johnson said.

According to the National Parkinson Foundation, around 1.5 million Americans suffer from Parkinson's disease, and some 60,000 new cases are diagnosed each year.

Source: AFP

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