Mitochondrial Dysfunction in Parkinson's Disease: Pathogenesis and Neuroprotection

Mitochondria are vitally important organelles involved in an array of functions. The most notable is their prominent role in energy metabolism, where they generate over 90% of our cellular energy in the form of ATP through oxidative phosphorylation. Mitochondria are involved in various other process...

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Main Authors: Ross B. Mounsey, Peter Teismann
Format: Article
Language:English
Published: Wiley 2011-01-01
Series:Parkinson's Disease
Online Access:http://dx.doi.org/10.4061/2011/617472
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author Ross B. Mounsey
Peter Teismann
author_facet Ross B. Mounsey
Peter Teismann
author_sort Ross B. Mounsey
collection DOAJ
description Mitochondria are vitally important organelles involved in an array of functions. The most notable is their prominent role in energy metabolism, where they generate over 90% of our cellular energy in the form of ATP through oxidative phosphorylation. Mitochondria are involved in various other processes including the regulation of calcium homeostasis and stress response. Mitochondrial complex I impairment and subsequent oxidative stress have been identified as modulators of cell death in experimental models of Parkinson's disease (PD). Identification of specific genes which are involved in the rare familial forms of PD has further augmented the understanding and elevated the role mitochondrial dysfunction is thought to have in disease pathogenesis. This paper provides a review of the role mitochondria may play in idiopathic PD through the study of experimental models and how genetic mutations influence mitochondrial activity. Recent attempts at providing neuroprotection by targeting mitochondria are described and their progress assessed.
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spelling doaj-art-8e6417856f2046a9a005d3eb4d1f72882025-08-20T02:09:22ZengWileyParkinson's Disease2042-00802011-01-01201110.4061/2011/617472617472Mitochondrial Dysfunction in Parkinson's Disease: Pathogenesis and NeuroprotectionRoss B. Mounsey0Peter Teismann1School of Medical Sciences, College of Life Sciences and Medicine, University of Aberdeen, Institute of Medical Sciences, Foresterhill, Aberdeen AB25 2ZD, UKSchool of Medical Sciences, College of Life Sciences and Medicine, University of Aberdeen, Institute of Medical Sciences, Foresterhill, Aberdeen AB25 2ZD, UKMitochondria are vitally important organelles involved in an array of functions. The most notable is their prominent role in energy metabolism, where they generate over 90% of our cellular energy in the form of ATP through oxidative phosphorylation. Mitochondria are involved in various other processes including the regulation of calcium homeostasis and stress response. Mitochondrial complex I impairment and subsequent oxidative stress have been identified as modulators of cell death in experimental models of Parkinson's disease (PD). Identification of specific genes which are involved in the rare familial forms of PD has further augmented the understanding and elevated the role mitochondrial dysfunction is thought to have in disease pathogenesis. This paper provides a review of the role mitochondria may play in idiopathic PD through the study of experimental models and how genetic mutations influence mitochondrial activity. Recent attempts at providing neuroprotection by targeting mitochondria are described and their progress assessed.http://dx.doi.org/10.4061/2011/617472
spellingShingle Ross B. Mounsey
Peter Teismann
Mitochondrial Dysfunction in Parkinson's Disease: Pathogenesis and Neuroprotection
Parkinson's Disease
title Mitochondrial Dysfunction in Parkinson's Disease: Pathogenesis and Neuroprotection
title_full Mitochondrial Dysfunction in Parkinson's Disease: Pathogenesis and Neuroprotection
title_fullStr Mitochondrial Dysfunction in Parkinson's Disease: Pathogenesis and Neuroprotection
title_full_unstemmed Mitochondrial Dysfunction in Parkinson's Disease: Pathogenesis and Neuroprotection
title_short Mitochondrial Dysfunction in Parkinson's Disease: Pathogenesis and Neuroprotection
title_sort mitochondrial dysfunction in parkinson s disease pathogenesis and neuroprotection
url http://dx.doi.org/10.4061/2011/617472
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