Cross-talk between mitochondria and proteasome in Parkinson’s disease pathogenesis
- 1 Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal
- 2 Faculty of Medicine, University of Coimbra, Coimbra, Portugal
Parkinson’s disease (PD) is the most common progressive neurodegenerative movement disorder, characterized by the selective loss of nigrostriatal dopaminergic neurons, and the presence of intracellular insoluble proteinaceous inclusions, known as Lewy Bodies. Although PD etiopathogenesis remains elusive, the leading hypothesis for the death of specific groups of neurons establishes that mitochondrial dysfunction, alterations in the ubiquitin-proteasomal system (UPS), and oxidative stress are major events that act synergistically causing this devastating disease. In this review we will focus on mitochondrial impairment and its implications on proteasomal function and alpha-synuclein aggregation. We will address the role of mitochondria and proteasome cross-talk in the neuronal loss that leads to PD and discuss how this knowledge might further improve patient therapy.
Keywords: Parkinson’s disease, dopamine, alpha-synuclein, mitochondria, proteasome
Citation: Branco DM, Arduino DM, Esteves AR, Silva DFF, Cardoso SM and Oliveira C (2010) Cross-talk between mitochondria and proteasome in Parkinson’s disease pathogenesis. Front. Ag. Neurosci. 2,17:1-10. doi: 10.3389/fnagi.2010.00017
Received: 31 December 2009;
Paper pending published: 18 January 2010;
Accepted: 12 April 2010; Published online: 21 May 2010.
Edited by:Paula I. Moreira, University of Coimbra, Portugal
Reviewed by:Tiago F. Outeiro, University of Lisbon, Portugal
Avi Friedlich, Harvard Medical School, USA
Copyright: © 2010 Branco, Arduino, Esteves, Silva, Cardoso and Oliveira. This is an open-access article subject to an exclusive license agreement between the authors and the Frontiers Research Foundation, which permits unrestricted use, distribution, and reproduction in any medium, provided the original authors and source are credited.
*Correspondence: Catarina Resende Oliveira, Center for Neuroscience and Cell Biology of Coimbra, University of Coimbra, 3004 Coimbra, Portugal. e-mail: email@example.com