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    Immunological features of alpha-synuclein in Parkinson's disease

    Roodveldt, C. and Christodoulou, John and Dobson, C.M. (2008) Immunological features of alpha-synuclein in Parkinson's disease. Journal of Cellular and Molecular Medicine 12 (5B), pp. 1820-1829. ISSN 1582-1838.

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    Abstract

    Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized pathologically by the presence, in the brain, of intra-cellular protein inclusions highly enriched in aggregated α-synuclein (αSyn), known as Lewy bodies. The onset of PD is accompanied by a local immune reaction in regions of the brain affected by the inclusions, although the mechanism that leads to pathogenesis is far from clear. It is, however, established that disease onset and progression are characterized by sustained activation of microglia, which is linked to significant dopaminergic neuron loss in the substantia nigra. A recent body of evidence indicates that aggregated or modified αSyn can indeed trigger the activation of microglia, inducing a lethal cascade of neuroinflammation and eventually, neuronal loss, pointing at aggregated and modified forms of αSyn as a primary cause of PD pathogenesis. By releasing toxic factors, or by phagocy-tosing neighbouring cells, activated microglia and astrocytes may form a self-perpetuating cycle for neuronal degeneration. Additional findings suggest a link between αSyn and humoural-mediated mechanisms in PD. In this review, we attempt to recapitulate our current understanding of PD physiopathology focused on αSyn and its links with the immune system, as well as of novel and promising therapeutic avenues for the treatment of PD and of other synucleinopathies.

    Metadata

    Item Type: Article
    School: Birkbeck Faculties and Schools > Faculty of Science > School of Natural Sciences
    Research Centres and Institutes: Structural Molecular Biology, Institute of (ISMB)
    Depositing User: Administrator
    Date Deposited: 04 Aug 2010 14:09
    Last Modified: 02 Aug 2023 16:49
    URI: https://eprints.bbk.ac.uk/id/eprint/1007

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