Abstract
Parkinson’s disease is the second most common neurodegenerative disorder characterized by persistent loss of dopaminergic neurons in the SN and clinically associated with cognitive, behavioral and motor deficits. There is an enormous amount of data that provides convincing evidence about the prime involvement of mitochondria in the onset and progression of neurodegeneration. Several studies have also emphasized that accumulation of toxic protein and their aggregates in mitochondria lead to energy deficits, excessive ROS generation, mutations in mitochondrial genome and proteins regulating mitochondrial homeostasis, and impaired mitochondrial dynamics in animal models of PD and patients. Here we discuss about the bioenergetic agents, which have been tested for reducing the mitochondrial dysfunction and associated disease pathology in cellular and animal models of PD and PD patients with encouraging outcomes. We also provide a succinct overview of current therapeutic implications of PGC-1α, SIRT, AMPK, and Nrf2-ARE as salutary targets to overcome the deleterious effects posed by mitochondrial dysfunction in the onset and progression of PD.
Keywords: Parkinson's disease, mitochondrial dysfunction, PGC-1α, sirtuins, creatine, coenzyme-Q10, triterpenoids, bioenergetic defects, neurodegenerative diseases.
Current Pharmaceutical Design
Title:Mitochondria: Prospective Targets for Neuroprotection in Parkinson's Disease
Volume: 20 Issue: 35
Author(s): Anuradha Yadav, Swati Agarwal, Shashi Kant Tiwari and Rajnish K. Chaturvedi
Affiliation:
Keywords: Parkinson's disease, mitochondrial dysfunction, PGC-1α, sirtuins, creatine, coenzyme-Q10, triterpenoids, bioenergetic defects, neurodegenerative diseases.
Abstract: Parkinson’s disease is the second most common neurodegenerative disorder characterized by persistent loss of dopaminergic neurons in the SN and clinically associated with cognitive, behavioral and motor deficits. There is an enormous amount of data that provides convincing evidence about the prime involvement of mitochondria in the onset and progression of neurodegeneration. Several studies have also emphasized that accumulation of toxic protein and their aggregates in mitochondria lead to energy deficits, excessive ROS generation, mutations in mitochondrial genome and proteins regulating mitochondrial homeostasis, and impaired mitochondrial dynamics in animal models of PD and patients. Here we discuss about the bioenergetic agents, which have been tested for reducing the mitochondrial dysfunction and associated disease pathology in cellular and animal models of PD and PD patients with encouraging outcomes. We also provide a succinct overview of current therapeutic implications of PGC-1α, SIRT, AMPK, and Nrf2-ARE as salutary targets to overcome the deleterious effects posed by mitochondrial dysfunction in the onset and progression of PD.
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Cite this article as:
Yadav Anuradha, Agarwal Swati, Tiwari Kant Shashi and Chaturvedi K. Rajnish, Mitochondria: Prospective Targets for Neuroprotection in Parkinson's Disease, Current Pharmaceutical Design 2014; 20 (35) . https://dx.doi.org/10.2174/1381612820666140305224545
DOI https://dx.doi.org/10.2174/1381612820666140305224545 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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