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dc.creatorDARBINIAN, Nune
dc.creatorSelzer, Michael
dc.date.accessioned2024-01-03T20:46:13Z
dc.date.available2024-01-03T20:46:13Z
dc.date.issued2021-08-04
dc.identifier.citationDarbinian, Nune; Selzer, Michael E. MD, PhD, FRCP,*. Oligodendrocyte pathology in fetal alcohol spectrum disorders. Neural Regeneration Research 17(3):p 497-502, March 2022. DOI: 10.4103/1673-5374.314294
dc.identifier.issn1876-7958
dc.identifier.urihttp://hdl.handle.net/20.500.12613/9466
dc.description.abstractThe pathology of fetal alcohol syndrome and the less severe fetal alcohol spectrum disorders includes brain dysmyelination. Recent studies have shed light on the molecular mechanisms underlying these white matter abnormalities. Rodent models of fetal alcohol syndrome and human studies have shown suppressed oligodendrocyte differentiation and apoptosis of oligodendrocyte precursor cells. Ethanol exposure led to reduced expression of myelin basic protein and delayed myelin basic protein expression in rat and mouse models of fetal alcohol syndrome and in human histopathological specimens. Several studies have reported increased expression of many chemokines in dysmyelinating disorders in central nervous system, including multiple sclerosis and fetal alcohol syndrome. Acute ethanol exposure reduced levels of the neuroprotective insulin-like growth factor-1 in fetal and maternal sheep and in human fetal brain tissues, while ethanol increased the expression of tumor necrosis factor α in mouse and human neurons. White matter lesions have been induced in the developing sheep brain by alcohol exposure in early gestation. Rat fetal alcohol syndrome models have shown reduced axon diameters, with thinner myelin sheaths, as well as reduced numbers of oligodendrocytes, which were also morphologically aberrant oligodendrocytes. Expressions of markers for mature myelination, including myelin basic protein, also were reduced. The accumulating knowledge concerning the mechanisms of ethanol-induced dysmyelination could lead to the development of strategies to prevent dysmyelination in children exposed to ethanol during fetal development. Future studies using fetal oligodendrocyte- and oligodendrocyte precursor cell-derived exosomes isolated from the mother’s blood may identify biomarkers for fetal alcohol syndrome and even implicate epigenetic changes in early development that affect oligodendrocyte precursor cell and oligodendrocyte function in adulthood. By combining various imaging modalities with molecular studies, it may be possible to determine which fetuses are at risk and to intervene therapeutically early in the pregnancy.
dc.format.extent6 pages
dc.languageEnglish
dc.language.isoeng
dc.relation.ispartofFaculty/ Researcher Works
dc.relation.haspartNeural Regeneration Research, Vol. 17, No. 3
dc.relation.isreferencedbyMedknow Publications
dc.rightsAttribution-NonCommercial-ShareAlike CC BY-NC-SA
dc.rights.urihttps://creativecommons.org/licenses/by-nc-sa/4.0/deed.en
dc.subjectAlcohol
dc.subjectDevelopment
dc.subjectDysmyelination
dc.subjectEthanol
dc.subjectFetal alcohol syndrome
dc.subjectFetal brain
dc.subjectMyelin basic protein
dc.subjectNeurodegeneration
dc.subjectOligodendrocyte injury
dc.subjectOligodendrocyte precursor cells
dc.titleOligodendrocyte pathology in fetal alcohol spectrum disorders
dc.typeText
dc.type.genreJournal article
dc.contributor.groupShriners Hospitals Pediatric Research Center (Temple University)
dc.relation.doihttp://dx.doi.org/10.4103/1673-5374.314294
dc.ada.noteFor Americans with Disabilities Act (ADA) accommodation, including help with reading this content, please contact scholarshare@temple.edu
dc.description.schoolcollegeLewis Katz School of Medicine
dc.creator.orcidDarbinian|0000-0002-8712-4940
dc.creator.orcidSelzer|0000-0002-1141-217X
dc.temple.creatorDarbinian, Nune
dc.temple.creatorSelzer, Michael E.
refterms.dateFOA2024-01-03T20:46:13Z


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