Protein That Controls Movement Does the Opposite in Parkinson's

Study with mice suggests it may be a new drug target

URL of this page: http://www.nlm.nih.gov/medlineplus/news/fullstory_121185.html
(*this news item will not be available after 04/24/2012)

By Robert Preidt

Wednesday, January 25, 2012

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Parkinson's Disease

WEDNESDAY, Jan. 25 (HealthDay News) -- Researchers who identified a protein that worsens symptoms of Parkinson's disease say their finding could eventually lead to new treatments for the neurodegenerative disease.

The protein, RGS4, normally helps regulate the activity in neurons in the striatum, the part of the brain that controls movement.

But in models of Parkinson's disease in mice, the researchers found that RGS4 actually contributes to problems with motor control, leading to a deterioration of movement and motor coordination.

The study, published online Jan. 25 in the journal Neuron, was conducted by scientists at the Gladstone Institutes, a nonprofit biomedical research organization affiliated with the University of California, San Francisco (UCSF).

It's long been known that decreased levels of the brain chemical dopamine are associated with Parkinson's.
Patients take a drug called Levodopa to increase dopamine levels but the drug's effectiveness begins to weaken as the disease progresses.

This has led scientists to start looking for potential new treatment targets.

"About 60,000 Americans are diagnosed with Parkinson's annually, and dopamine-based therapies often do not provide a long-term solution," Anatol Kreitzer, a Gladstone investigator and an assistant professor of physiology and neurology at UCSF, said in a Gladstone news release.

"Our discovery that RGS4 may play a role in the development of Parkinson's symptoms helps us lay the groundwork for a new therapeutic strategy -- independent of dopamine," he claimed.

While studies involving animals can be promising, they frequently fail to produce similar results in humans.

SOURCE: Gladstone Institutes, news release, Jan. 25, 2012

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