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Parkinson's disease: Excess of special protein identified as key to symptoms and possible new target for treatment with widely used anti-cancer drug imatinib
Date:10/1/2010

Johns Hopkins scientists have discovered that the over-activation of a single protein may shut down the brain-protecting effects of a molecule and facilitate the most common form of Parkinson's disease. The finding of this mechanism could lead to important new targets for drugs already known to inhibit it, thus controlling symptoms of the disorder, which affects about 1 million older Americans.

Previous research demonstrated that a protein called parkin protects brain cells by "tagging" certain toxic elements that are then destroyed naturally. It was also known that mutations in the gene that holds the code for parkin cause rare, familial forms of PD. However, parkin's role remained unclear in sporadic late-onset PD, the prevalence of which is increasing as the population ages.

Results of the new study, published Sept. 7 in the Proceedings of the National Academy of Sciences (PNAS) Online Early Edition, indicate that an over-activation of a protein called c-Abl can shut down the activity of parkin and contribute to a build-up of toxic proteins that kill brain cells and enables the progression of PD.

C-Abl contributes to the regulation of cell death and is implicated in a host of diseases. It has already has proven to be a target for certain types of cancer-killing drugs, such as imatinib (Gleevec), the first drug designed to directly switch off a biochemical signal that directly targets a protein vital to cancer growth, says Ted Dawson, M.D., Ph.D., Leonard and Madlyn Abramson Professor in Neurodegenerative Diseases and scientific director of the Johns Hopkins Institute for Cell Engineering.

"Our new appreciation of c-Abl's role in sporadic PD suggests that we can give brain-permeable inhibitors of c-Abl to maintain parkin's normal protective function," Dawson says. "The testing of these already approved, well-tolerated drugs for a new use as a neuro-protective treatment for PD is a potentially exciting the
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Contact: Maryalice Yakutchik
myakutc1@jhmi.edu
443-287-2251
Johns Hopkins Medical Institutions
Source:Eurekalert

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