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When mistreated children act out later in life: Brain gene may play a role, study says

This news release is also available in French.

Variations in a gene that helps regulate several behavior-related brain chemicals may partly explain why some mistreated children later develop antisocial behavior, while others do not, according to an international study. The authors, from the U.K., the U.S., and New Zealand, report their findings in the journal Science, published by the American Association for the Advancement of Science.

If their findings can be replicated, they may help efforts to identify children with a particular risk for developing behavior problems or committing crimes as adults, said study author Terrie Moffitt of King's College London and the University of Wisconsin. Because there are so many degrees of antisocial behavior, the researchers expect many additional gene-environment interactions to be involved.

"This is not really the story of a gene that has a risk for antisocial behavior. It's the story of the interplay between a gene and the experience of maltreatment," Moffit said.

Among the males in the study, those who had a variation of a certain gene and had experienced childhood maltreatment made up 12 percent of the whole male population. They made up 22 percent of the group that became antisocial as adults, however. That makes the combination a significant risk factor for antisocial behavior, comparable to the major risk factors for heart disease, according to the researchers.

Moffitt and her colleagues studied the MAOA gene, which encodes an enzyme that works on several different neurotransmitters, the chemical messengers that hop from one neuron to another.

"In its normal role, the enzyme has a sort of clean-up function. It stays in the synapse between two neurons and clears away excess neurotransmitters. I think of it as a little Pacman," Moffitt said.

A common variation of the gene produces
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Contact: Lisa Onaga
lonaga@aaas.org
202-326-7088
American Association for the Advancement of Science
1-Aug-2002


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