If the change happens early, it may explain how the brain adapts and could be a potential treatment target, he said. If it shows up later, it could be from the toxic effects of alcohol. We need to further define its role.
The researchers studied postmortem brain tissue samples from 14 male chronic alcoholics and 14 age-matched male individuals with no history of alcohol abuse. The samples were from the superior frontal cortex, an area of the brain associated with alcohol abuse that is a part of the brain pathway that involves feelings of desire and reward.
This protein may play a role in the reward circuitry, said Gu. If that is true, a drug to block these effects could reduce dependence on alcohol.
In addition to their findings about beta-catenin, the scientists also found higher levels of Myc, a protein that at high levels can cause a transformation of cells that leads to cancer. The findings could help explain a link between alcohol and cancer.
The results may help to explain why excessive alcohol consumption increases the risk of cancer, said Gu. While an association has been established between alcohol consumption and various cancers, the mechanism remains obscure. Because the production of Myc in the cell is regulated by beta-catenin, our findings may suggest that alcohol activates beta-catenin production; that in turn activates Myc production, and that ultimately leads to cell transformation and cancer.
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| Contact: Karen Richardson krchrdsn@wfubmc.edu 336-716-4453 Wake Forest University Baptist Medical Center Source:Eurekalert |