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  • Nrf2 and Parkinson's Disease

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    TodorovicPUB3824.pdf (273.5Kb)
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    Author(s)
    Todorovic, Michael
    Mellick, George
    Griffith University Author(s)
    Mellick, George
    Todorovic, Michael
    Year published
    2016
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    Abstract
    Parkinson’s disease (PD) results from a complex interaction of environmental and genetic influences on a background of aging. Regardless of etiology, significant clinical advances rely on identifying the common biological pathways that underpin neuronal degeneration. Oxidative stress is consistently reported as a hallmark feature of PD. Recently, it has been demonstrated that Nrf2 modulation can protect neurons from parkinsonian agents and, in some instances, reverse motor symptoms of animal models. Furthermore, baseline aberrations of Nrf2 and its associated pathway have been reported in PD patients, and genetic variability—within ...
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    Parkinson’s disease (PD) results from a complex interaction of environmental and genetic influences on a background of aging. Regardless of etiology, significant clinical advances rely on identifying the common biological pathways that underpin neuronal degeneration. Oxidative stress is consistently reported as a hallmark feature of PD. Recently, it has been demonstrated that Nrf2 modulation can protect neurons from parkinsonian agents and, in some instances, reverse motor symptoms of animal models. Furthermore, baseline aberrations of Nrf2 and its associated pathway have been reported in PD patients, and genetic variability—within and around the Nrf2 gene— may modify PD susceptibility and onset. Overall, Nrf2 dysregulation has been tentatively implicated in the pathogenesis of PD and may prove to be an effective therapeutic target.
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    Book Title
    A Master Regulator of Oxidative Stress - The Transcription Factor Nrf2
    DOI
    https://doi.org/10.5772/65450
    Copyright Statement
    © 2016 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
    Subject
    Cell Neurochemistry
    Publication URI
    http://hdl.handle.net/10072/143569
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