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Research Gets Closer to Origin of Parkinson's Disease
Date:1/4/2008

a-synuclein -- as opposed to modified forms -- also block the desired breakdown of damaged nerve cell molecules. Such mutant proteins are present in the 5 percent to 10 percent of Parkinson's patients struck with a relatively rare, familial form of the disease.

"But the novelty of our work today is that the modified protein mechanism we found this time will apply to all Parkinson's patients," noted Cuervo. "And so it becomes possible that in the future we can design drugs to improve the function of the garbage containers, the lysosomes, in all Parkinson's patients, and maybe overcome the problem that these nerve cells have handling the modified molecules."

Cuervo and her Einstein colleagues conducted the study, based on laboratory work with male rats, in collaboration with scientists from Columbia University in New York City, the University of Pennsylvania, and Harvard Medical School in Boston.

The National Parkinson Foundation estimates that 1.5 million Americans are affected with Parkinson's disease, the most common degenerative brain disorder affecting movement.

The nerve damage that's characteristic of this incurable disease brings about a dramatic loss of muscle control, typically manifesting as tremors, stiffness, and a loss of balance and agility.

Though optimistic about her work, Cuervo emphasized that translating the latest findings into new preventive and curative interventions will require a lot more research and time.

"I want to be very cautious," she said. "We are far from a final cure. It's not something we can do tomorrow. It's going to take some time. But now we know what the problem is. And we think that we have something, a target, to focus on."

Nonetheless, Dr. Robert Burke, director of the Morris K. Udall Parkinson's Disease Research Center of Excellence at Columbia University, called the new findings a "big step forward."

"Their first finding was only related to the
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