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Updated: May 14, 2026

Histological Examination of Mitochondrial Morphology in a Parkinson's Disease Model
Published on: June 23, 2023
Parkinson's disease: a complex interplay of mitochondrial DNA alterations and oxidative stress
Sarah Ciccone1, Emiliano Maiani, Giovanna Bellusci
1Department of Biology, University of Rome "Tor Vergata", Via della Ricerca Scientifica, 00133 Rome, Italy. stefania.gonfloni@uniroma2.it.
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.
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