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Extracellular Interactions of Alpha-Synuclein in Multiple System Atrophy

Valdinocci, Dario; Radford, Rowan A W; Goulding, Michael; Hayashi, Junna; Chung, Roger S; Pountney, Dean L

Description

Multiple system atrophy, characterized by atypical Parkinsonism, results from central nervous system (CNS) cell loss and dysfunction linked to aggregates of the normally pre-synaptic α-synuclein protein. Mostly cytoplasmic pathological α-synuclein inclusion bodies occur predominantly in oligodendrocytes in affected brain regions and there is evidence that α-synuclein released by neurons is taken up preferentially by oligodendrocytes. However, extracellular α-synuclein has also been shown to...[Show more]

dc.contributor.authorValdinocci, Dario
dc.contributor.authorRadford, Rowan A W
dc.contributor.authorGoulding, Michael
dc.contributor.authorHayashi, Junna
dc.contributor.authorChung, Roger S
dc.contributor.authorPountney, Dean L
dc.date.accessioned2019-03-05T22:56:45Z
dc.date.available2019-03-05T22:56:45Z
dc.identifier.issn1661-6596
dc.identifier.urihttp://hdl.handle.net/1885/156989
dc.description.abstractMultiple system atrophy, characterized by atypical Parkinsonism, results from central nervous system (CNS) cell loss and dysfunction linked to aggregates of the normally pre-synaptic α-synuclein protein. Mostly cytoplasmic pathological α-synuclein inclusion bodies occur predominantly in oligodendrocytes in affected brain regions and there is evidence that α-synuclein released by neurons is taken up preferentially by oligodendrocytes. However, extracellular α-synuclein has also been shown to interact with other neural cell types, including astrocytes and microglia, as well as extracellular factors, mediating neuroinflammation, cell-to-cell spread and other aspects of pathogenesis. Here, we review the current evidence for how α-synuclein present in the extracellular milieu may act at the cell surface to drive components of disease progression. A more detailed understanding of the important extracellular interactions of α-synuclein with neuronal and non-neuronal cell types both in the brain and periphery may provide new therapeutic targets to modulate the disease process.
dc.description.sponsorshipWe acknowledge NHMRC Dementia Teams Grant funding to RSC (APP1095215).
dc.format20 pages
dc.format.mimetypeapplication/pdf
dc.language.isoen_AU
dc.publisherMDPI
dc.rights© 2018 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 (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
dc.sourceInternational journal of molecular sciences
dc.subjectchaperone
dc.subjectgliosis
dc.subjectglymphatic
dc.subjectmultiple system atrophy
dc.subjectneuroinflammation
dc.subjectα-synuclein
dc.titleExtracellular Interactions of Alpha-Synuclein in Multiple System Atrophy
dc.typeJournal article
local.identifier.citationvolume19
dcterms.dateAccepted2018-12-19
dc.date.issued2018-12-19
local.identifier.ariespublicationu3102795xPUB2411
local.publisher.urlhttps://www.mdpi.com/
local.type.statusPublished Version
local.contributor.affiliationHayashi, Junna, Research School of Chemistry, Australian National University
dc.relationhttp://purl.org/au-research/grants/nhmrc/APP1095215
local.identifier.essn1422-0067
local.bibliographicCitation.issue12
local.bibliographicCitation.startpage4129
local.identifier.doi10.3390/ijms19124129
dcterms.accessRightsOpen Access
CollectionsANU Research Publications

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