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January 12, 2007|Volume 35, Number 14|Two-Week Issue


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Team maps gene for nicotine
dependence to chromosome 5

Genes that appear to increase the risk of nicotine dependence are likely to be found on several locations, including a region of chromosome 5, according to a Yale School of Medicine study in Biological Psychiatry.

"These data add to the growing evidence for specific locations for genes that influence risk for nicotine dependence," says Joel Gelernter, professor of psychiatry, genetics and neurobiology, and lead author of the study. "The chromosome 5 linkage signal is our most remarkable result statistically."

He says the finding is significant since any ability to predict nicotine dependence based on genes that influence risk could be useful and might help reduce the number of persons who begin smoking. The World Health Organization estimates that more than one billion people smoke, and the number is continuing to increase.

"Nicotine dependence, like alcohol, cocaine and opioid dependence, is heritable," Gelernter says. "It has been estimated that 60% or more of tobacco use is associated with heritable factors. We are using genetic linkage analysis that can be used to identify genomic risk loci."

The study population included 634 small nuclear families with multiple individuals affected by cocaine or opioid dependence. Most also provided nicotine dependence information. Study subjects came from two ethnic backgrounds -- European Americans and African Americans.

The results showed there were a number of loci that appeared to contribute to risk and one distinct difference between the two groups. The researchers also found one significant genome-wide linkage on chromosome 5 for the African Americans and a strong linkage on chromosome 7 for European Americans.

The overall pattern of results supports the interpretation that at least some genetic determinants of nicotine dependence overlap between different, differently ascertained populations," Gelernter says. "The chromosome 5 finding in African Americans might be more specific to this sample, either because of the population or because of the way the sample was ascertained."

Co-authors include Dr. Michael Krauthammer and James Poling of Yale; Dr. Henry Kranzler of the University of Connecticut Medical School; Dr. Roger Weiss of Harvard; Carolien Panhuysen and Lindsay Farrer of Boston University; and Dr. Kathleen Brady of the Medical University of South Carolina.

The work was supported by the National Institutes of Health and the U.S. Department of Veterans Affairs.

-- By Jacqueline Weaver


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