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When cells run out of fuel
Date:8/24/2009

nduce Parkinson's disease. The relevance of mitochondria to the loss of neurons seems plausible after all, mitochondria supply the cells with energy in form of adenosine triphosphate and play a substantial role in the regulation of cell death.

The scientists' results now combine both observations on a genetic basis. They found that the Parkinson-associated genes PINK1 and Parkin functionally interact to maintain mitochondrial function. Loss of Parkin or PINK1 function impairs the morphology and activity of mitochondria, which then produce less adenosine triphosphate. "Our results also confirm the high neuroprotective potential of Parkin", Winklhofer says. "We observed that Parkin can compensate a loss of PINK1 function, but not the other way round". Winklhofer and her colleagues have shown earlier that Parkin can protect neurons under various stress conditions.

Until today, there is no possibility to prevent or cure Parkinson's disease. All pharmacological approaches are merely symptomatic and aim at replacing the neurotransmitter dopamine. Insight into the function of Parkinson-associated genes can help to identify new targets for therapeutic strategies in order to prevent or halt the loss of dopamine-producing neurons. So far, six Parkinson-associated genes are known whose functions remain to be elucidated in detail. In the case of Parkin and PINK1 scientists have made significant steps forward and now aim at uncovering the molecular mechanisms of their functions.


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Contact: Dr. Konstanze F. Winklhofer
konstanze.winklhofer@med.uni-muenchen.de
49-892-180-75483
Ludwig-Maximilians-Universitt Mnchen
Source:Eurekalert

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