Next Article in Journal
Regeneration of Articular Cartilage in Lizard Knee from Resident Stem/Progenitor Cells
Next Article in Special Issue
The Role of Mitochondrial DNA in Mediating Alveolar Epithelial Cell Apoptosis and Pulmonary Fibrosis
Previous Article in Journal
Biogas Production from Sugarcane Waste: Assessment on Kinetic Challenges for Process Designing
Previous Article in Special Issue
Mitochondrial Transcription Factor A and Mitochondrial Genome as Molecular Targets for Cisplatin-Based Cancer Chemotherapy
Article Menu
Issue 9 (September) cover image

Export Article

Open AccessReview
Int. J. Mol. Sci. 2015, 16(9), 20704-20730; doi:10.3390/ijms160920704

Mitochondria: A Therapeutic Target for Parkinson’s Disease?

1
Department of Neurological Surgery, Case Western Reserve University, Cleveland, OH 44106, USA
2
Department of Physiology, Case Western Reserve University, Cleveland, OH 44106, USA
*
Authors to whom correspondence should be addressed.
Academic Editors: Jaime M. Ross and Giuseppe Coppotelli
Received: 10 June 2015 / Revised: 14 August 2015 / Accepted: 20 August 2015 / Published: 1 September 2015
(This article belongs to the Special Issue Mitochondrial Dysfunction in Ageing and Diseases)
View Full-Text   |   Download PDF [727 KB, uploaded 1 September 2015]

Abstract

Parkinson’s disease (PD) is one of the most common neurodegenerative disorders. The exact causes of neuronal damage are unknown, but mounting evidence indicates that mitochondrial-mediated pathways contribute to the underlying mechanisms of dopaminergic neuronal cell death both in PD patients and in PD animal models. Mitochondria are organized in a highly dynamic tubular network that is continuously reshaped by opposing processes of fusion and fission. Defects in either fusion or fission, leading to mitochondrial fragmentation, limit mitochondrial motility, decrease energy production and increase oxidative stress, thereby promoting cell dysfunction and death. Thus, the regulation of mitochondrial dynamics processes, such as fusion, fission and mitophagy, represents important mechanisms controlling neuronal cell fate. In this review, we summarize some of the recent evidence supporting that impairment of mitochondrial dynamics, mitophagy and mitochondrial import occurs in cellular and animal PD models and disruption of these processes is a contributing mechanism to cell death in dopaminergic neurons. We also summarize mitochondria-targeting therapeutics in models of PD, proposing that modulation of mitochondrial impairment might be beneficial for drug development toward treatment of PD. View Full-Text
Keywords: Parkinson’s disease; mitochondrial dysfunction; mitochondrial dynamics Parkinson’s disease; mitochondrial dysfunction; mitochondrial dynamics
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. (CC BY 4.0).

Scifeed alert for new publications

Never miss any articles matching your research from any publisher
  • Get alerts for new papers matching your research
  • Find out the new papers from selected authors
  • Updated daily for 49'000+ journals and 6000+ publishers
  • Define your Scifeed now

SciFeed Share & Cite This Article

MDPI and ACS Style

Luo, Y.; Hoffer, A.; Hoffer, B.; Qi, X. Mitochondria: A Therapeutic Target for Parkinson’s Disease? Int. J. Mol. Sci. 2015, 16, 20704-20730.

Show more citation formats Show less citations formats

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top