Int. J. Mol. Sci. 2013, 14(2), 2388-2409; doi:10.3390/ijms14022388
Parkinson’s Disease: A Complex Interplay of Mitochondrial DNA Alterations and Oxidative Stress
Sarah Ciccone 1, Emiliano Maiani 1, Giovanna Bellusci 1, Marc Diederich 2,3
and Stefania Gonfloni 1,2,*
and Stefania Gonfloni 1,2,*
1
Department of Biology, University of Rome "Tor Vergata", Via della Ricerca Scientifica, 00133 Rome, Italy
2
Laboratoire de Biologie Moléculaire et Cellulaire du Cancer, Kirchberg Hospital, 9 Rue Edward Steichen, 2540 Luxembourg, Luxembourg
3
College of Pharmacy, Seoul National University, 599 Gwanak-ro, Gwanak-gu, Seoul 151-742, Korea
*
Author to whom correspondence should be addressed.
Received: 5 December 2012 / Revised: 14 January 2013 / Accepted: 21 January 2013 / Published: 24 January 2013
(This article belongs to the Special Issue DNA Damage and Repair in Degenerative Diseases)
Abstract
Parkinson’s disease (PD) is one of the most common age-related neurodegenerative diseases. This pathology causes a significant loss of dopaminergic neurons in the Substantia Nigra. Several reports have claimed a role of defective nuclear and mitochondrial DNA repair pathways in PD etiology, in particular, of the Base Excision Repair (BER) system. In addition, recent findings, related to PD progression, indicate that oxidative stress pathways involving c-Abl and GST could also be implicated in this pathology. This review focuses on recently described networks most likely involved in an integrated manner in the course of PD. View Full-TextKeywords:
neurodegenerative diseases; Parkinson’s disease (PD); base excision repair (BER); mitochondria; oxidative stress; reactive oxidative species (ROS); reactive nitrogen species (RNS); c-Abl; reduced glutathione (GSH); oxidized glutathione (GSS-)
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Ciccone, S.; Maiani, E.; Bellusci, G.; Diederich, M.; Gonfloni, S. Parkinson’s Disease: A Complex Interplay of Mitochondrial DNA Alterations and Oxidative Stress. Int. J. Mol. Sci. 2013, 14, 2388-2409.
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