Using proteomics analysis of brain tissue samples, scientists in the US and Australia have found that the beta-catenin signal transduction pathway is upregulated in alcoholism, according to a report in the June issue of Alcoholism: Clinical and Experimental Research.We have identified a protein that may be a cause of alcohol dependence and tolerance, suggesting the possibility of developing a drug to inhibit the molecule and treat the disease, senior author Dr. Qiang Gu said in a press release from Wake Forest University School of Medicine in Winston-Salem, North Carolina. Dr. Gu and colleagues used an antibody micro-array assay to study brain expression of 17 proteins associated with beta-catenin signaling cascades in 14 chronic alcoholics and 14 age- and gender-matched controls. Postmortem samples were obtained from the superior frontal cortices, one of the brain regions most vulnerable to chronic alcohol abuse. Levels of both alpha- and beta-catenin were significantly increased in samples from alcoholics, as was the level of the beta-catenin down stream gene product Myc. These observations suggest that beta-catenin could directly participate in regulation of synaptic function in key brain circuits that are central to alcohol abusive behaviors, Dr. Gu and his associates suggest.Conversely, an upregulation of beta-catenin and Myc levels could be a protective mechanism to minimize alcohol-induced brain damage and neuronal loss. The finding that the Myc proto-oncogene is also upregulated in alcoholism may explain the strong association between chronic and excessive alcohol consumption and various cancers, the authors indicate. Summing up, Dr. Gu's team concludes that the beta-catenin signal transduction pathway may play a significant role in alcohol-induced neuroadaptation in the brain.
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