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dc.contributor.authorDuce, JA
dc.contributor.authorWong, BX
dc.contributor.authorDurham, H
dc.contributor.authorDevedjian, J-C
dc.contributor.authorSmith, DP
dc.contributor.authorDevos, D
dc.date.accessioned2021-02-04T01:55:33Z
dc.date.available2021-02-04T01:55:33Z
dc.date.issued2017-06-07
dc.identifierpii: 10.1186/s13024-017-0186-8
dc.identifier.citationDuce, J. A., Wong, B. X., Durham, H., Devedjian, J. -C., Smith, D. P. & Devos, D. (2017). Post translational changes to alpha-synuclein control iron and dopamine trafficking; a concept for neuron vulnerability in Parkinson's disease. MOLECULAR NEURODEGENERATION, 12 (1), https://doi.org/10.1186/s13024-017-0186-8.
dc.identifier.issn1750-1326
dc.identifier.urihttp://hdl.handle.net/11343/259520
dc.description.abstractParkinson's disease is a multifactorial neurodegenerative disorder, the aetiology of which remains elusive. The primary clinical feature of progressively impaired motor control is caused by a loss of midbrain substantia nigra dopamine neurons that have a high α-synuclein (α-syn) and iron content. α-Syn is a neuronal protein that is highly modified post-translationally and central to the Lewy body neuropathology of the disease. This review provides an overview of findings on the role post translational modifications to α-syn have in membrane binding and intracellular vesicle trafficking. Furthermore, we propose a concept in which acetylation and phosphorylation of α-syn modulate endocytic import of iron and vesicle transport of dopamine during normal physiology. Disregulated phosphorylation and oxidation of α-syn mediate iron and dopamine dependent oxidative stress through impaired cellular location and increase propensity for α-syn aggregation. The proposition highlights a connection between α-syn, iron and dopamine, three pathological components associated with disease progression in sporadic Parkinson's disease.
dc.languageEnglish
dc.publisherBMC
dc.rights.urihttps://creativecommons.org/licenses/by/4.0
dc.titlePost translational changes to alpha-synuclein control iron and dopamine trafficking; a concept for neuron vulnerability in Parkinson's disease
dc.typeJournal Article
dc.identifier.doi10.1186/s13024-017-0186-8
melbourne.affiliation.departmentFlorey Department of Neuroscience and Mental Health
melbourne.affiliation.departmentBiochemistry and Molecular Biology
melbourne.affiliation.facultyMedicine, Dentistry & Health Sciences
melbourne.source.titleMolecular Neurodegeneration
melbourne.source.volume12
melbourne.source.issue1
dc.rights.licenseCC BY
melbourne.elementsid1215048
melbourne.contributor.authorDuce, James
melbourne.contributor.authorWong, Bruce
dc.identifier.eissn1750-1326
melbourne.accessrightsOpen Access


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