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Updated: Jul 16, 2026

Histological Examination of Mitochondrial Morphology in a Parkinson's Disease Model
Published on: June 23, 2023
Mitochondrial dysfunction in Parkinson's disease
Jiro Fukae1, Yoshikuni Mizuno, Nobutaka Hattori
1Department of Neurology, Juntendo University School of Medicine, 2-1-1 Hongo, Tokyo 113-8421, Japan.
Abstract:
Parkinson's disease (PD) is one of the most common neurodegenerative disorders characterized by resting tremor, rigidity, and bradykinesia. The primary cause of PD is still unknown, but oxidative stress and mitochondrial dysfunction have been implicated as important contributors to neuronal death in substantia nigra (SN) of PD. Considering neurons as post-mitotic cells, neurons could have error-avoiding mechanism against oxidative DNA damage. Indeed, several DNA repairing enzymes such as MTH1, OGG1, and MUTYH express in human brain. All the three enzymes up-regulated in the SN of PD patients, suggesting these three enzymes cooperate in mitochondrial DNA repairing in PD brain.
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