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Study illuminates birth defects caused by copper deficiency

t underlies Menkes disease, the researchers reported. They further showed that insertion of a normal human copy of the ATP7A gene reversed the development defects in the mutant fish.

The discovery of the Menkes fish will now permit screens of pharmaceutical compounds that restore copper enzyme function in the setting of a deficiency of ATP7A, the researchers said. Such drugs would be of immediate clinical relevance for treating Menkes disease.

Similar studies in zebrafish that examine the role of other gene-nutrient interactions in early human development could ultimately lead to improvements in prenatal care with the capacity to reduce the risk of birth defects, the researchers said.

"While it will require an enormous amount of science, this is the first time it is even within our grasp to know how an individual woman's genes might affect her nutritional requirements and the risk that her children might develop a congenital disorder," Gitlin said. "Ultimately, that information could allow us to provide for every woman a recipe for what is right for her pregnancy."


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Contact: Heidi Hardman
hhardman@cell.com
617-397-2879
Cell Press
8-Aug-2006


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