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Newcastle University scientists lead the way in uncovering the ‘alcoholics’ gene’

Scientists from Newcastle have helped discover which gene controls how much alcohol we drink – and how if it breaks down it can lead to alcoholism.

The study found that normal mice show no interest in booze and would much rather sup from a bottle of water if given the choice.

But rodents with a mutation in their Gabrb1 gene overwhelmingly preferred drinking booze, choosing to consume almost 85% of their daily fluids as drinks containing alcohol as strong as wine.

“It’s amazing to think that a small change in the code for just one gene can have such profound effects on complex behaviours like alcohol consumption,” said Dr Quentin Anstee, a consultant liver specialist at Newcastle University, who was joint lead author of the study.

“We are continuing our work to establish whether the gene has a similar influence in humans, though we know that in people alcoholism is much more complicated as environmental factors come into play.

“But there is the real potential for this to guide development of better treatments for alcoholism in the future.”

The consortium of researchers involved came from five UK universities – Newcastle University, Imperial College London,  Sussex University, University College London and University of Dundee – as well as the MRC Mammalian Genetics Unit at Harwell.

Their work was funded by the Medical Research Council (MRC), the Wellcome Trust and ERAB, with their findings published in the journal Nature Communications.

The research showed that mice carrying a mutation were willing to work to obtain the alcohol-containing drink by pushing a lever and, unlike normal mice, continued to do so even over long periods. They would voluntarily consume sufficient alcohol in an hour to get drunk and would even have difficulty in coordinating their movements.

The cause of the excessive drinking was tracked down to single mutation in the gene Gabrb1, which codes for an important part of a receptor in the brain. The researchers found that the gene mutation caused the receptor to activate spontaneously even when the usual trigger was not present, and these changes were particularly strong in the region of the brain that controls pleasurable emotions and reward.

“The mutation of the receptor is alters its structure and creates spontaneous electrical activity in the brain in this pleasure zone, the nucleus accumbens,” Dr Anstee said.

“As the electrical signal from these receptors increases, so does the desire to drink to such an extent that mice will actually work to get the alcohol, for much longer than we would have expected.”

Professor Hugh Perry, chair of the MRC’s Neurosciences and Mental Health Board, said he hoped the research, which has taken 10 years, could lead to better treatment for alcoholism in the future.

“Alcohol addiction places a huge burden on the individual, their family and wider society,” he said.

“There’s still a great deal we don’t understand about how and why consumption progresses into addiction, but the results of this long-running project suggest that, in some individuals, there may be a genetic component.

“If further research confirms that a similar mechanism is present in humans, it could help us to identify those most at risk of developing an addiction and ensure they receive the most effective treatment.”

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