UQ biochemists are working with American researchers to pinpoint why only some parts of the brain are damaged in alcoholics.
Associate Professor Peter Dodd and his team from UQ's School of Molecular and Microbial Sciences has secured a five-year, $1.23 million grant from the United States' biomedical funding arm, the National Institute of Health (NIH) to find out.
Chronic alcohol abuse kills brain cells in the front of the brain, which affect planning, and social interactions and inhibitions.
The UQ team with collaborators from The University of Texas, want to find out what makes these cells so vulnerable.
Professor Dodd said his team was analysing brain tissue from dead alcoholics, mostly Anglo-Celtic men who've averaged more than 10 drinks a day.
The group analyses samples using a microarray analysis, a process they pioneered with human brain samples in 2000.
From a DNA sample applied to a microscope slide, the microarray computer produces about 50,000 coloured spots showing which genes are expressed or switched on in the sample.
"What we're trying to find out is, what's different in the superior frontal cortex [front of brain] when you compare alcoholics with controls, that's not different in a spared area of the brain," Dr Dodd said.
"In that way we can start to find those messages that show altered expression in the area of the brain that shows the pathology."
He said the microarray analysis could be useful for many neurological diseases.
"It's got general applicability to neurological diseases, because most neurological diseases also exhibit regional selectivity of pathology."
Professor Dodd said researching proteins was the next step as that would tell them why some cells have impaired function.
He has also teamed up with United Kingdom colleagues to find out why people get addicted to alcohol -- with the long-term goal of producing a drug that could reduce alcohol dependence.
Source: Eurekalert & othersLast reviewed: By John M. Grohol, Psy.D. on 21 Feb 2009
Published on PsychCentral.com. All rights reserved.
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