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dc.contributor.authorLewohl, Joanneen_US
dc.contributor.authorWixey, Julieen_US
dc.contributor.authorG. Harper, Cliveen_US
dc.contributor.authorR. Dodd, Peteren_US
dc.date.accessioned2017-04-24T08:31:13Z
dc.date.available2017-04-24T08:31:13Z
dc.date.issued2005en_US
dc.date.modified2009-03-26T06:40:54Z
dc.identifier.issn01456008en_US
dc.identifier.doi10.1097/01.alc.0000179406.98868.59en_AU
dc.identifier.urihttp://hdl.handle.net/10072/21901
dc.description.abstractBackground: Chronic and excessive alcohol misuse results in neuropathological damage in the cerebral cortex. The damage includes white matter loss, brain atrophy, and selective loss of neurons in the superior frontal gyrus. Chronic alcohol misuse also results in alterations in the expression of a number of genes, including a selective reprogramming of myelin gene expression in the frontal cortex. Methods: The expression of cyclic nucleotide phosphodiesterase, glial fibrillary acidic protein, myelin-associated glycoprotein, myelin basic protein, and myelin proteolipid protein were assessed in the superior frontal gyrus and the primary motor cortex of control, uncomplicated alcoholic, and cirrhotic alcoholic cases. Results: Overall, the expression of cyclic nucleotide phosphodiesterase, glial fibrillary acidic protein, myelin-associated glycoprotein, and myelin basic protein were significantly lower in the cirrhotic alcoholic cases compared with controls, with a similar tendency for myelin proteolipid protein. There was a strong correlation between the expression of the proteins studied and the brain weight of the individual case, but this interaction did not confound the overall analysis. There was no significant difference between controls and uncomplicated alcoholics. Conclusions: The loss of myelin proteins occurred without gross changes in brain pathology or brain weight and was not restricted to pathologically susceptible brain regions. It is not possible to determine whether the loss of myelin proteins in cirrhotic alcoholics is the result of cirrhosis per se or the combination of alcohol misuse and liver cirrhosis. Future studies comparing cases with alcoholic and nonalcoholic cirrhosis of the liver disease are required to elucidate this further.en_US
dc.description.peerreviewedYesen_US
dc.description.publicationstatusYesen_AU
dc.languageEnglishen_US
dc.language.isoen_AU
dc.publisherWilliams and Wilkinsen_US
dc.publisher.placeUnited Statesen_US
dc.relation.ispartofstudentpublicationNen_AU
dc.relation.ispartofpagefrom1698en_US
dc.relation.ispartofpageto1705en_US
dc.relation.ispartofissue9en_US
dc.relation.ispartofjournalAlcoholism, clinical and experimental researchen_US
dc.relation.ispartofvolume29en_US
dc.rights.retentionYen_AU
dc.subject.fieldofresearchcode270502en_US
dc.subject.fieldofresearchcode270201en_US
dc.subject.fieldofresearchcode320702en_US
dc.titleExpression of MBP, PLP, MAG, CNP and GFAP in the Human Alcoholic Brainen_US
dc.typeJournal articleen_US
dc.type.descriptionC1 - Peer Reviewed (HERDC)en_US
dc.type.codeC - Journal Articlesen_US
gro.facultyGriffith Health, School of Medical Scienceen_US
gro.date.issued2005
gro.hasfulltextNo Full Text


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