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Mitochondria and Parkinsonís Disease

By September 3, 2009

Some forms of familial Parkinsonís disease are linked to loss of function of the genes called Parkin, or PINK1, but, until recently, it was not understood why. Why did these genetic defects lead to PD in some families? Recent evidence suggests that these genes are important for normal functioning of the mitochondria. Mitochondria are those cellular processes in every cell of your body that produce energy for the bodyís functions. The mitochondria produce energy in the form of adenosine triphosate. Cells, particularly cells that produce dopamine, need this energy molecule in order to perform their normal functions. Scientists have long suspected that damage to the mitochondria in your cells can contribute to the onset of PD. When mitochondria are damaged in animals, it can produce a form of parkinsonism. Now scientists have discovered that Parkinson-associated genes like 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. Slowly, the pieces to the puzzle are being put together. Already scientists are talking about creating drugs or genetic products that can protect mitochondria and thus treat or ameliorate PD.


Source: Lutz, A.K., Exner, N., Fett, M.E., Schlehe, J.S., Kloos, K., Laemmermann, K., Brunner, B., Kurz-Drechsler, A., Vogel, F., Reichert, A.S., Bouman, L., Vogt-Weisenhorn, D., Wurst, W., Tatzelt, J., Haass, C., and Winkelhofer, K.F. Loss of parkin or PINK1 function increases DRP1-independent mitochondrial fragmentation. Journal of Biological Chemistry, 21. August 2009, Vol. 284, Issue 34, 22938-22951.

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