α-SYNUCLEINOPATHY PHENOTYPES McCann, Heather en_US Stevens, Claire H en_US Cartwright, Heidi en_US Halliday, Glenda en_US 2021-11-25T12:29:09Z 2021-11-25T12:29:09Z 2014 en_US
dc.description.abstract α-Synucleinopathies are neurodegenerative diseases characterised by the abnormal accumulation of α-synuclein aggregates in neurons, nerve fibres or glial cells. While small amounts of these α-synuclein pathologies can occur in some neurologically normal individuals who do not have associated neurodegeneration, the absence of neurodegeneration in such individuals precludes them from having a degenerative α-synucleinopathy, and it has yet to be established whether such individuals have a form of preclinical disease. There are three main types of α-synucleinopathy, Parkinson’s disease (PD), dementia with Lewy bodies (DLB), and multiple system atrophy (MSA), with other rare disorders also having α-synuclein pathologies, such as various neuroaxonal dystrophies. Multiple clinical phenotypes exist for each of the three main α-synucleinopathies, with these phenotypes differing in the dynamic distribution of their underlying neuropathologies. Identifying the factors involved in causing different α-synuclein phenotypes may ultimately lead to more targeted therapeutics as well as more accurate clinical prognosis. en_US
dc.identifier.issn 1353-8020 en_US
dc.language English
dc.language.iso EN en_US
dc.rights CC BY-NC-ND 3.0 en_US
dc.rights.uri en_US
dc.source Legacy MARC en_US
dc.subject.other multiple system atrophy en_US
dc.subject.other α-synuclein en_US
dc.subject.other dementia with Lewy bodies en_US
dc.subject.other Parkinson’s disease en_US
dc.type Journal Article en
dcterms.accessRights open access
dspace.entity.type Publication en_US
unsw.description.publisherStatement NOTICE: this is the author’s version of a work that was accepted for publication in Parkinsonism and Related Disorders. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Parkinsonism and Related Disorders, Vol. 20, Suppl. 1, (2014) DOI 10.1016/S1353-8020(13)70017-8 en_US
unsw.identifier.doiPublisher en_US
unsw.relation.faculty Medicine & Health
unsw.relation.ispartofissue Suppl. 1 en_US
unsw.relation.ispartofjournal Parkinsonism and Related Disorders en_US
unsw.relation.ispartofpagefrompageto S62-S67 en_US
unsw.relation.ispartofvolume 20 en_US
unsw.relation.originalPublicationAffiliation McCann, Heather, NeuRA en_US
unsw.relation.originalPublicationAffiliation Stevens, Claire H, Neuroscience Research Australia, Faculty of Medicine, UNSW en_US
unsw.relation.originalPublicationAffiliation Cartwright, Heidi, Neuroscience Research Australia, Faculty of Medicine, UNSW en_US
unsw.relation.originalPublicationAffiliation Halliday, Glenda, Neuroscience Research Australia, Faculty of Medicine, UNSW en_US Neuroscience Research Australia *
unsw.subject.fieldofresearchcode 110903 Central Nervous System en_US
Original bundle
Now showing 1 - 1 of 1
Thumbnail Image
Author's postprint.pdf
527.05 KB
Resource type