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dc.contributor.authorvan Tilborg, Erik
dc.contributor.authorde Theije, Caroline GM
dc.contributor.authorvan Hal, Maurik
dc.contributor.authorWagenaar, Nienke
dc.contributor.authorde Vries, Linda S
dc.contributor.authorBenders, Manon J
dc.contributor.authorRowitch, David
dc.contributor.authorNijboer, Cora H
dc.date.accessioned2018-06-15T14:30:15Z
dc.date.available2018-06-15T14:30:15Z
dc.date.issued2018-02
dc.identifier.issn0894-1491
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/277111
dc.description.abstractInfants born prematurely are at high risk to develop white matter injury (WMI), due to exposure to hypoxic and/or inflammatory insults. Such perinatal insults negatively impact the maturation of oligodendrocytes (OLs), thereby causing deficits in myelination. To elucidate the precise pathophysiology underlying perinatal WMI, it is essential to fully understand the cellular mechanisms contributing to healthy/normal white matter development. OLs are responsible for myelination of axons. During brain development, OLs are generally derived from neuroepithelial zones, where neural stem cells committed to the OL lineage differentiate into OL precursor cells (OPCs). OPCs, in turn, develop into premyelinating OLs and finally mature into myelinating OLs. Recent studies revealed that OPCs develop in multiple waves and form potentially heterogeneous populations. Furthermore, it has been shown that myelination is a dynamic and plastic process with an excess of OPCs being generated and then abolished if not integrated into neural circuits. Myelination patterns between rodents and humans show high spatial and temporal similarity. Therefore, experimental studies on OL biology may provide novel insights into the pathophysiology of WMI in the preterm infant and offers new perspectives on potential treatments for these patients.
dc.description.sponsorshipThis work was funded by the Wilhelmina Children's Hospital Research Fund and the Brain Foundation Netherlands.
dc.languageeng
dc.publisherWiley
dc.rightsAttribution 4.0 International
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectbrain development
dc.subjectmyelination
dc.subjectoligodendrocyte precursor cells
dc.subjectpreterm birth
dc.subjectwhite matter injury
dc.titleOrigin and dynamics of oligodendrocytes in the developing brain: Implications for perinatal white matter injury.
dc.typeArticle
prism.endingPage238
prism.issueIdentifier2
prism.publicationDate2018
prism.publicationNameGlia
prism.startingPage221
prism.volume66
dc.identifier.doi10.17863/CAM.24403
dcterms.dateAccepted2017-10-20
rioxxterms.versionofrecord10.1002/glia.23256
rioxxterms.versionVoR
rioxxterms.licenseref.urihttp://creativecommons.org/licenses/by/4.0/
rioxxterms.licenseref.startdate2018-02
dc.contributor.orcidRowitch, David [0000-0002-0079-0060]
dc.identifier.eissn1098-1136
rioxxterms.typeJournal Article/Review
pubs.funder-project-idMedical Research Council (MC_PC_12009)
cam.issuedOnline2017-11-14


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Attribution 4.0 International
Except where otherwise noted, this item's licence is described as Attribution 4.0 International