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

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

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.

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.

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"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.

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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.

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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