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New Insights into the Evolution of Parkinson’s Disease

In a study conducted within the context of the German national genomics network (NGFN), researchers from the Hertie-Institute for clinical neuroscience have been the first to demonstrate that the two proteins associated with Parkinson’s Disease, PINK1 and Parkin, regulate the disposal of damaged mitochondria and in which way this is done. The Tübingen scientists’ hypothesis: a disruption in this disposal mechanism could be involved in the emergence of Parkinson’s Disease. (Online pre-release on January 24th 2010 in Nature Cell Biology)

Every cell is equipped with many mitochondria, which are cell organelles providing the cell with high-energy molecules essential for survival. Pathological or damaged mitochondria however, cease the production of energy. They cause intensified damage of the cell by increased oxidative stress, leading up to cellular necrosis. The disposal of faulty mitochondria (mitochondrial autophagy or mitophagy) enables cleaning of the cell and protects it from flawed mitochondria and their destructive ramifications.

The scientists were able to demonstrate that mutations associated with Parkinson’s inhibit the sequential process of disposal at certain points. The enzymatic function of the mitochondrial kinase PINK1 is essential and facilitates a quick recruitment and adhesion of the Parkin protein to the damaged mitochondria. Parkin’s enzymatic activity in turn allows for the tagging of VDAC1 with Ubiquitin, a protein serving as signal molecule for the disposal of proteins modified in this way.
Interestingly, VDAC1 forms a channel through the mitochondria’s outer membrane and is already suspected to contribute heavily to cell necrosis when mitochondria are faulty.

Contact Information:
Universitätsklinikum Tübingen
Zentrum für Neurologie
Hertie-Institut für klinische Hirnforschung (HIH)
Partnerstandort Deutsches Zentrum für Neurodegenerative Erkrankungen (DZNE)
Prof. Dr. Philipp Kahle
+49 7071 2981-970
philipp.kahle@uni-tuebingen.de

Topic: Health and Medicine
Source: NGFN

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	Common New Insights into the Evolution of Parkinson’s Disease In a study conducted within the context of the German national genomics network (NGFN), researchers from the Hertie-Institute for clinical neuroscience have been the first to demonstrate that the two proteins associated with Parkinson’s Disease, PINK1 and Parkin, regulate the disposal of damaged mitochondria and in which way this is done. The Tübingen scientists’ hypothesis: a disruption in this disposal mechanism could be involved in the emergence of Parkinson’s Disease. (Online pre-release on January 24th 2010 in Nature Cell Biology) Every cell is equipped with many mitochondria, which are cell organelles providing the cell with high-energy molecules essential for survival. Pathological or damaged mitochondria however, cease the production of energy. They cause intensified damage of the cell by increased oxidative stress, leading up to cellular necrosis. The disposal of faulty mitochondria (mitochondrial autophagy or mitophagy) enables cleaning of the cell and protects it from flawed mitochondria and their destructive ramifications. The scientists were able to demonstrate that mutations associated with Parkinson’s inhibit the sequential process of disposal at certain points. The enzymatic function of the mitochondrial kinase PINK1 is essential and facilitates a quick recruitment and adhesion of the Parkin protein to the damaged mitochondria. Parkin’s enzymatic activity in turn allows for the tagging of VDAC1 with Ubiquitin, a protein serving as signal molecule for the disposal of proteins modified in this way. Interestingly, VDAC1 forms a channel through the mitochondria’s outer membrane and is already suspected to contribute heavily to cell necrosis when mitochondria are faulty. Contact Information: Universitätsklinikum Tübingen Zentrum für Neurologie Hertie-Institut für klinische Hirnforschung (HIH) Partnerstandort Deutsches Zentrum für Neurodegenerative Erkrankungen (DZNE) Prof. Dr. Philipp Kahle +49 7071 2981-970 philipp.kahle@uni-tuebingen.de Topic: Health and Medicine Source: NGFN	Print page Back