[caldeerster]

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.

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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