Parkinson’s Disease: A Complex Interplay of Mitochondrial DNA Alterations and Oxidative Stress

International Journal of Molecular Sciences

Sarah Ciccone²  Emiliano Maiani²  Giovanna Bellusci²  Marc Diederich¹ 

[1] Laboratoire de Biologie Moléculaire et Cellulaire du Cancer, Kirchberg Hospital, 9 Rue Edward Steichen, 2540 Luxembourg, Luxembourg; E-Mail:;Department of Biology, University of Rome “Tor Vergata”, Via della Ricerca Scientifica, 00133 Rome, Italy; E-Mails:

关键词: 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-);   

DOI  :  10.3390/ijms14022388

来源: mdpi

【 摘 要 】

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.

【 授权许可】

CC BY   
© 2013 by the authors; licensee Molecular Diversity Preservation International, Basel, Switzerland.