Expression of MBP, PLP, MAG, CNP and GFAP in the Human Alcoholic Brain

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Title Expression of MBP, PLP, MAG, CNP and GFAP in the Human Alcoholic Brain
Author Lewohl, Joanne Marie; Wixey, Julie; Harper, Clive G.; Dodd, Peter R.
Journal Name Alcoholism, clinical and experimental research
Year Published 2005
Place of publication United States
Publisher Williams And Wilkins
Abstract Background: 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.
Peer Reviewed Yes
Published Yes
Alternative URI http://dx.doi.org/10.1097/01.alc.0000179406.98868.59
Volume 29
Issue Number 9
Page from 1698
Page to 1705
ISSN 0145-6008
Date Accessioned 2006-07-10
Date Available 2009-03-26T06:40:54Z
Language en_AU
Research Centre Griffith Health Institute; Molecular Basis of Disease
Faculty Griffith Health Faculty
Subject PRE2009-Central Nervous System; PRE2009-Gene Expression; PRE2009-Neurobiology
URI http://hdl.handle.net/10072/21901
Publication Type Journal Articles (Refereed Article)
Publication Type Code c1a

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