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dc.contributor.authorZirngibl, Martin
dc.contributor.authorAssinck, Peggy
dc.contributor.authorSizov, Anastasia
dc.contributor.authorCaprariello, Andrew V
dc.contributor.authorPlemel, Jason R
dc.date.accessioned2022-05-09T11:05:05Z
dc.date.available2022-05-09T11:05:05Z
dc.date.issued2022-05-07
dc.date.submitted2021-10-28
dc.identifier.issn1750-1326
dc.identifier.others13024-022-00538-8
dc.identifier.other538
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/336920
dc.descriptionFunder: Canadian Institutes for Health Research (CA)
dc.descriptionFunder: Natural Sciences and Engineering Research Council of Canada; doi: http://dx.doi.org/10.13039/501100000038
dc.descriptionFunder: Fondation Brain Canada; doi: http://dx.doi.org/10.13039/100009408
dc.descriptionFunder: Azrieli Foundation; doi: http://dx.doi.org/10.13039/501100005155
dc.description.abstractBACKGROUND: The dietary consumption of cuprizone - a copper chelator - has long been known to induce demyelination of specific brain structures and is widely used as model of multiple sclerosis. Despite the extensive use of cuprizone, the mechanism by which it induces demyelination are still unknown. With this review we provide an updated understanding of this model, by showcasing two distinct yet overlapping modes of action for cuprizone-induced demyelination; 1) damage originating from within the oligodendrocyte, caused by mitochondrial dysfunction or reduced myelin protein synthesis. We term this mode of action 'intrinsic cell damage'. And 2) damage to the oligodendrocyte exerted by inflammatory molecules, brain resident cells, such as oligodendrocytes, astrocytes, and microglia or peripheral immune cells - neutrophils or T-cells. We term this mode of action 'extrinsic cellular damage'. Lastly, we summarize recent developments in research on different forms of cell death induced by cuprizone, which could add valuable insights into the mechanisms of cuprizone toxicity. With this review we hope to provide a modern understanding of cuprizone-induced demyelination to understand the causes behind the demyelination in MS.
dc.languageen
dc.publisherSpringer Science and Business Media LLC
dc.subjectReview
dc.subjectCuprizone
dc.subjectMultiple Sclerosis
dc.subjectDemyelination
dc.subjectOligodendrocytes
dc.subjectInflammation
dc.subjectCell death
dc.subjectAstrocytes
dc.subjectMicroglia
dc.subjectCNS
dc.titleOligodendrocyte death and myelin loss in the cuprizone model: an updated overview of the intrinsic and extrinsic causes of cuprizone demyelination.
dc.typeArticle
dc.date.updated2022-05-09T11:05:04Z
prism.issueIdentifier1
prism.publicationNameMol Neurodegener
prism.volume17
dc.identifier.doi10.17863/CAM.84339
dcterms.dateAccepted2022-04-08
rioxxterms.versionofrecord10.1186/s13024-022-00538-8
rioxxterms.versionVoR
rioxxterms.licenseref.urihttp://creativecommons.org/licenses/by/4.0/
dc.identifier.eissn1750-1326
cam.issuedOnline2022-05-07


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