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.
Keywords: 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-)
This is an open access article distributed under the
Creative Commons Attribution License which permits unrestricted use, distribution,
and reproduction in any medium, provided the original work is properly cited.
Export to BibTeX
MDPI and ACS Style
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.
Ciccone S, Maiani E, Bellusci G, Diederich M, Gonfloni S. Parkinson’s Disease: A Complex Interplay of Mitochondrial DNA Alterations and Oxidative Stress. International Journal of Molecular Sciences. 2013; 14(2):2388-2409.
Ciccone, Sarah; Maiani, Emiliano; Bellusci, Giovanna; Diederich, Marc; Gonfloni, Stefania. 2013. "Parkinson’s Disease: A Complex Interplay of Mitochondrial DNA Alterations and Oxidative Stress." Int. J. Mol. Sci. 14, no. 2: 2388-2409.