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Excess of Protein Used as Anti-cancer Drug Triggers Parkinson's Disease

by Tanya Thomas on  October 4, 2010 at 11:07 AM Cancer News   - G J E 4
A new study has found that over-activation of a single protein may shut down the brain-protecting effects of a molecule and increases the likeliness of the most common form of Parkinson's disease.
 Excess of Protein Used as Anti-cancer Drug Triggers  Parkinson's Disease
Excess of Protein Used as Anti-cancer Drug Triggers Parkinson's Disease
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Johns Hopkins scientists found this mechanism that may lead to important new targets for drugs already known to inhibit it, thus controlling symptoms of the disorder.

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Previous research demonstrated that a protein called parkin protects brain cells by 'tagging' certain toxic elements that are then destroyed naturally.

However, the results of the new study have indicated 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 proven to be a target for certain types of cancer-killing drugs, such as imatinib (Gleevec) said Ted Dawson.

"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.

"The testing of these already approved, well-tolerated drugs for a new use - as a neuro-protective treatment for PD - is a potentially exciting therapeutic arc that should be pursued," said Dawson.

The researchers first used a test called the Western blot to label certain proteins in neuron-like human cells in culture. They could see that c-Abl shut down the activity of parkin by measuring the levels of chemical tags on proteins that, in a healthy system, are marked for destruction.

These "garbage" proteins, when overabundant, have been shown previously by Dawson's lab to be selectively toxic to neurons. When c-Abl was active, parkin's ability to tag those proteins was significantly decreased.

Next, using a mouse, which had been given drugs, that cause Parkinson's-like traits, the team proved that when c-Abl is activated, parkin's function shuts down and as a result, garbage proteins accumulate and lead to a significant loss of neurons.

Finally, the scientists turned to human brain tissue to look for evidence that c-Abl are a major regulator of parkin function. By comparing brain tissue of patients who died with Parkinson's disease with those who died of other causes, they established that when c-Abl shuts down Parkin, the "garbage" proteins accumulate and result is the death of neurons.

The findings were published in the Proceedings of the National Academy of Sciences (PNAS).

Source: ANI
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