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This article is part of the supplement: Proceedings of the 2011 International Conference on Molecular Neurodegeneration

Open Access Lecture presentation

Molecular pathways to Parkinson’s disease

Ming Guo

  • Correspondence: Ming Guo

Author Affiliations

Department of Neurology, Department of Molecular & Medical Pharmacology, Brain Research Institute, UCLA David Geffen School of Medicine, LA, California, USA

Molecular Neurodegeneration 2012, 7(Suppl 1):L13  doi:10.1186/1750-1326-7-S1-L13


The electronic version of this article is the complete one and can be found online at: http://www.molecularneurodegeneration.com/content/7/S1/L13


Published:7 February 2012

© 2012 Guo; licensee BioMed Central Ltd.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Background

Parkinson’s disease (PD) is the second most common neurodegenerative disease. Mutations in PINK1 and PARKIN result in familial forms of PD. We have found that lack of pink1 or parkin in Drosophila results in defects in mitochondrial integrity in multiple tissues. Flies lacking PINK1 or parkin show highly similar, if not identical, phenotypes.

Results

Genetic studies suggest that PINK1 and parkin function in a common genetic pathway with PINK1 positively regulating parkin. The PINK1/parkin pathway regulates mitochondrial dynamics by positively regulating drp1 and negatively regulating mitofusin. Mammalian cell-based studies suggest that the PINK1/parkin may regulate mitochondrial quality control via mitophagy. How autophagy intersects with mitochondrial dynamics in vivo will be discussed.