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  • Interactions between calcium and alpha-synuclein in neurodegeneration

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    Author(s)
    Rcom-H'cheo-Gauthier, Alex
    Goodwin, Jacob
    Pountney, Dean L
    Griffith University Author(s)
    Pountney, Dean L.
    Goodwin, Jacob
    Rcom-H'cheo-Gauthier, Alexandre N.
    Year published
    2014
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    Abstract
    In Parkinson's disease and some atypical Parkinson's syndromes, aggregation of the a-synuclein protein (a-syn) has been linked to neurodegeneration. Many triggers for pathological a-syn aggregation have been identified, including port-translational modifications, oxidative stress and raised metal ions, such as Ca2+. Recently, it has been found using cell culture models that transient increases of intracellular Ca2+ induce cytoplasmic a-syn aggregates. Ca2+-dependent a-syn aggregation could be blocked by the Ca2+ buffering agent, BAPTA-AM, or by the Ca2+ channel blocker, Trimethadione. Furthermore, a greater proportion of ...
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    In Parkinson's disease and some atypical Parkinson's syndromes, aggregation of the a-synuclein protein (a-syn) has been linked to neurodegeneration. Many triggers for pathological a-syn aggregation have been identified, including port-translational modifications, oxidative stress and raised metal ions, such as Ca2+. Recently, it has been found using cell culture models that transient increases of intracellular Ca2+ induce cytoplasmic a-syn aggregates. Ca2+-dependent a-syn aggregation could be blocked by the Ca2+ buffering agent, BAPTA-AM, or by the Ca2+ channel blocker, Trimethadione. Furthermore, a greater proportion of cells positive for aggregates occurred when both raised Ca2+ and oxidative stress were combined, indicating that Ca2+ and oxidative stress cooperatively promote a-syn aggregation. Current on-going work using a unilateral mouse lesion model of Parkinson's disease shows a greater proportion of calbindin-positive neurons survive the lesion, with intracellular a-syn aggregates almost exclusively occurring in calbindin-negative neurons. These and other recent findings are reviewed in the context of neurodegenerative pathologies and suggest an association between raised Ca2+, a-syn aggregation and neurotoxicity.
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    Journal Title
    Biomolecules
    Volume
    4
    Issue
    3
    DOI
    https://doi.org/10.3390/biom4030795
    Copyright Statement
    © 2014 by the authors; licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/).
    Subject
    Cell Neurochemistry
    Biochemistry and Cell Biology
    Publication URI
    http://hdl.handle.net/10072/146902
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    • Journal articles

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