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  • Neuroinflammation in multiple system atrophy: Response to and cause of α-synuclein aggregation

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    VieiraPUB1876.pdf (840.7Kb)
    Author(s)
    Di MarcoVieira, Bruno
    Radford, Rowan A
    Chung, Roger S
    Guillemin, Gilles J
    Pountney, Dean L
    Griffith University Author(s)
    Pountney, Dean L.
    Vieira, Bruno DM.
    Year published
    2015
    Metadata
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    Abstract
    Multiple system atrophy (MSA) is a progressive neurodegenerative disease presenting with combinations of autonomic dysfunction, parkinsonism, cerebellar ataxia and/or pyramidal signs. Oligodendroglial cytoplasmic inclusions (GCIs) rich in α-synuclein (α-syn) constitute the disease hallmark, accompanied by neuronal loss and activation of glial cells which indicate neuroinflammation. Recent studies demonstrate that α-syn may be released from degenerating neurons to mediate formation of abnormal inclusion bodies and to induce neuroinflammation which, interestingly, might also favor the formation of intracellular α-syn aggregates ...
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    Multiple system atrophy (MSA) is a progressive neurodegenerative disease presenting with combinations of autonomic dysfunction, parkinsonism, cerebellar ataxia and/or pyramidal signs. Oligodendroglial cytoplasmic inclusions (GCIs) rich in α-synuclein (α-syn) constitute the disease hallmark, accompanied by neuronal loss and activation of glial cells which indicate neuroinflammation. Recent studies demonstrate that α-syn may be released from degenerating neurons to mediate formation of abnormal inclusion bodies and to induce neuroinflammation which, interestingly, might also favor the formation of intracellular α-syn aggregates as a consequence of cytokine release and the shift to a pro-inflammatory environment. Here, we critically review the relationships between α-syn and astrocytic and microglial activation in MSA to explore the potential of therapeutics which target neuroinflammation.
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    Journal Title
    Frontiers in Cellular Neuroscience
    Volume
    9
    DOI
    https://doi.org/10.3389/fncel.2015.00437
    Copyright Statement
    © 2015 Vieira, Radford, Chung, Guillemin and Pountney. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution and reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
    Subject
    Neurosciences not elsewhere classified
    Biochemistry and Cell Biology
    Neurosciences
    Publication URI
    http://hdl.handle.net/10072/141467
    Collection
    • Journal articles

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