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  • Alpha-synuclein is upregulated in neurones in response to chronic oxidative stress and is associated with neuroprotection

    Author(s)
    Quilty, MC
    King, AE
    Gai, W-P
    Pountney, DL
    West, AK
    Vickers, JC
    Dickson, TC
    Griffith University Author(s)
    Pountney, Dean L.
    Year published
    2006
    Metadata
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    Abstract
    Chronic oxidative stress has been linked to the neurodegenerative changes characteristic of Parkinson's disease, particularly alpha-synuclein accumulation and aggregation. However, it remains contentious whether these alpha-synuclein changes are cytotoxic or neuroprotective. The current study utilised long-term primary neural culture techniques with antioxidant free media to study the cellular response to chronic oxidative stress. Cells maintained in antioxidant free media were exquisitely more vulnerable to acute exposure to hydrogen peroxide, yet exposure of up to 10 days in antioxidant free media did not lead to ...
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    Chronic oxidative stress has been linked to the neurodegenerative changes characteristic of Parkinson's disease, particularly alpha-synuclein accumulation and aggregation. However, it remains contentious whether these alpha-synuclein changes are cytotoxic or neuroprotective. The current study utilised long-term primary neural culture techniques with antioxidant free media to study the cellular response to chronic oxidative stress. Cells maintained in antioxidant free media were exquisitely more vulnerable to acute exposure to hydrogen peroxide, yet exposure of up to 10 days in antioxidant free media did not lead to morphological alterations in neurones or glia. However, a subpopulation of neurones demonstrated a significant increase in the level of alpha-synuclein expressed within the cell body and at synaptic sites. This subset of neurones was also more resistant to apoptotic changes following exposure to antioxidant free media relative to other neurones. These data indicate that increased alpha-synuclein content is associated with neuroprotection from relatively low levels of oxidative stress.
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    Journal Title
    Experimental Neurology
    Volume
    199
    Issue
    2
    Publisher URI
    http://www.elsevier.com/locate/yexnr
    DOI
    https://doi.org/10.1016/j.expneurol.2005.10.018
    Subject
    Clinical sciences
    Neurosciences
    Publication URI
    http://hdl.handle.net/10072/14236
    Collection
    • Journal articles

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