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dc.contributor.authorRcom-H'cheo-Gauthier, Alexandre Nayen_US
dc.contributor.authorMeedeniya, Adrian Cuda Bandaen_US
dc.contributor.authorPountney, Dean Louisen_US
dc.date.accessioned2014-07-04en_US
dc.date.accessioned2014-11-10T03:19:13Z
dc.date.accessioned2017-03-02T00:40:59Z
dc.date.available2014-11-10T03:19:13Z
dc.date.available2017-03-02T00:40:59Z
dc.date.issued2014en_US
dc.identifier.urihttp://hdl.handle.net/10072/64453
dc.description.abstractIntroduction: Neurodegeneration in Parkinson’s disease is associated with protein aggregation and the formation of neuronal Lewy bodies mainly composed of the protein alpha-synuclein. Alpha-synuclein has been shown to aggregate when intracellular calcium levels are elevated. Moreover, the calcium buffering protein, Calbindin, the expression of which results in relative sparing of Calbindin-positive neurons in PD, may provide a degree of protection against the pathological process in Parkinson’s disease, pointing to the influence of calcium dysregulation in neurodegeneration. Methods: Unilateral lesioning of the medial forebrain bundle of C57 black mice with the mitochondrial inhibitor, rotenone, was performed to induce oxidative stress and stimulate neurodegeneration. Fluorescence immunohistochemistry of brain tissue was used to determine the frequency of Calbindin-28K positive cells and alpha-synuclein aggregates. Results: Confocal microscopy of mouse brain tissue sections showed more frequent Calbindin-28K positive cells within the lesioned hemisphere (p, 0.05) than within the control hemisphere. The data indicates more frequent alpha-synuclein aggregates within the lesioned hemisphere, and that aggregates are less numerous in Calbindin-positive cells. Conclusion: These findings suggest an association between the calcium buffering protein, Calbindin-28K, and neuronal survival and alpha-synuclein aggregation in a mouse model of Parkinson’s disease and implicate the involvement of calcium dysregulation in Parkinson’s disease.en_US
dc.description.peerreviewedNoen_US
dc.description.publicationstatusYesen_US
dc.format.extent72335 bytes
dc.format.mimetypeapplication/pdf
dc.publisherAustralasian Neuroscience Societyen_US
dc.publisher.placeAdelaideen_US
dc.publisher.urihttp://www.aomevents.com/ANS2014en_US
dc.relation.ispartofstudentpublicationNen_US
dc.relation.ispartofconferencename34th Annual Meeting of the Australasian Neuroscience Societyen_US
dc.relation.ispartofconferencetitle34th Annual Meeting of the Australasian Neuroscience Societyen_US
dc.relation.ispartofdatefrom2014-01-28en_US
dc.relation.ispartofdateto2014-01-31en_US
dc.relation.ispartoflocationAdelaideen_US
dc.rights.retentionYen_US
dc.subject.fieldofresearchNeurology and Neuromuscular Diseasesen_US
dc.subject.fieldofresearchcode110904en_US
dc.titleInvestigation of the Involvment of Calcium Regulation in the Unilateral Rotenone-Lesioned Mouse Model of Parkinson's Diseaseen_US
dc.typeConference output
dc.type.descriptionConference Publications (Extract Paper)en_US
dc.type.codee3en_US
gro.facultyGriffith Health Facultyen_US
gro.rights.copyright© The Author(s) 2014. The attached file is reproduced here in accordance with the copyright policy of the publisher. For information about this conference please refer to the conference’s website or contact the authors.en_US
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gro.griffith.authorRcom-H'cheo-Gauthier, Alexandre N.
gro.griffith.authorMeedeniya, Adrian C.
gro.griffith.authorPountney, Dean L.


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