Supported by the National Institute of Alcoholism and Alcohol Abuse (USA; National Institutes of Health grants AA12404 and AA012725-04) and the National Health and Medical Research Council (Australia).
Expression of MBP, PLP, MAG, CNP, and GFAP in the Human Alcoholic Brain
Article first published online: 3 MAY 2006
Alcoholism: Clinical and Experimental Research
Volume 29, Issue 9, pages 1698–1705, September 2005
How to Cite
Lewohl, J. M., Wixey, J., Harper, C. G. and Dodd, P. R. (2005), Expression of MBP, PLP, MAG, CNP, and GFAP in the Human Alcoholic Brain. Alcoholism: Clinical and Experimental Research, 29: 1698–1705. doi: 10.1097/01.alc.0000179406.98868.59
- Issue published online: 3 MAY 2006
- Article first published online: 3 MAY 2006
- Submitted for publication September 15, 2004; accepted June 13, 2005.
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.
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.
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.
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.