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dc.contributor.authorRcom-H'cheo-Gauthier, Alexandre N
dc.contributor.authorOsborne, Samantha L
dc.contributor.authorMeedeniya, Adrian CB
dc.contributor.authorPountney, Dean L
dc.date.accessioned2018-01-12T12:31:09Z
dc.date.available2018-01-12T12:31:09Z
dc.date.issued2016
dc.identifier.issn1662-453X
dc.identifier.doi10.3389/fnins.2016.00570
dc.identifier.urihttp://hdl.handle.net/10072/337307
dc.description.abstractAggregation of the pre-synaptic protein, α-synuclein (α-syn), is the key etiological factor in Parkinson's disease (PD) and other alpha-synucleinopathies, such as multiple system atrophy (MSA) and Dementia with Lewy bodies (DLB). Various triggers for pathological α-syn aggregation have been elucidated, including post-translational modifications, oxidative stress, and binding of metal ions, such as calcium. Raised neuronal calcium levels in PD may occur due to mitochondrial dysfunction and/or may relate to calcium channel dysregulation or the reduced expression of the neuronal calcium buffering protein, calbindin-D28k. Recent results on human tissue and a mouse oxidative stress model show that neuronal calbindin-D28k expression excludes α-syn inclusion bodies. Previously, cell culture model studies have shown that transient increases of intracellular free Ca(II), such as by opening of the voltage-gated plasma calcium channels, could induce cytoplasmic aggregates of α-syn. Raised intracellular free calcium and oxidative stress also act cooperatively to promote α-syn aggregation. The association between raised neuronal calcium, α-syn aggregation, oxidative stress, and neurotoxicity is reviewed in the context of neurodegenerative α-syn disease and potential mechanism-based therapies.
dc.description.peerreviewedYes
dc.languageEnglish
dc.publisherFrontiers Research Foundation
dc.relation.ispartofpagefrom1
dc.relation.ispartofpageto8
dc.relation.ispartofissue570
dc.relation.ispartofjournalFrontiers in Neuroscience
dc.relation.ispartofvolume10
dc.subject.fieldofresearchNeurosciences not elsewhere classified
dc.subject.fieldofresearchNeurosciences
dc.subject.fieldofresearchPsychology
dc.subject.fieldofresearchCognitive Sciences
dc.subject.fieldofresearchcode110999
dc.subject.fieldofresearchcode1109
dc.subject.fieldofresearchcode1701
dc.subject.fieldofresearchcode1702
dc.titleCalcium: Alpha-synuclein interactions in alpha synucleinopathies
dc.typeJournal article
dc.type.descriptionC1 - Articles
dc.type.codeC - Journal Articles
dcterms.licensehttp://creativecommons.org/licenses/by/4.0/
dc.description.versionPublished
gro.facultyGriffith Health, School of Medical Science
gro.rights.copyright© 2016 Rcom-H'cheo-Gauthier, Osborne, Meedeniya and Pountney. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or 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.
gro.hasfulltextFull Text
gro.griffith.authorPountney, Dean L.
gro.griffith.authorMeedeniya, Adrian C.
gro.griffith.authorRcom-H'cheo-Gauthier, Alexandre N.
gro.griffith.authorOsborne, Samantha L.


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