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Autistic behavior has genetic basis in mice

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A new mouse model of autism adds to growing evidence that genetics is a strong factor, if not the strongest, driving the neural development disorder.

Researchers at the University of California, San Francisco, bred a group of normal mice with a line of genetically modified mice that had a mouse version of autism. Of the 400 descendants of that crossbreeding, some had normal genes and some had irregular ones.

Researchers observed the behavior of the descended mice and found that specific autistic behaviors were associated with certain chromosomal regions. These regions contain genes associated with abnormal brain development and activity. The findings were published online in the open-access journal PLoS ONE.

"Having the genes means that you can begin to pick apart the connection between the genes and the actual behavior, and look at how the mutation on a gene might result in aberrant behavior," said co-senior author, Dr. Elliott Sherr, a pediatric neurologist at UCSF Benioff Children's Hospital and professor of neurology at UC San Francisco, in a statement.

The cause of autism has long puzzled scientists, but previous research strongly suggests that some people are genetically predisposed to the disorder. In family studies, researchers have found that autistic people are more likely to have autistic siblings, and twins are very likely to share autistic traits. Still, some believe that the condition may be linked to environmental factors; having an animal model will allow scientists to test for such effects.

Eventually, Sherr hopes to test new autism drugs in the mouse model. The National Institutes of Health and Pfizer ($PFE) provided funds to support the study.

Another recent study, published in Human Molecular Genetics, found that children with autism have increased levels of genetic change in certain "hotspots"--regions of the genome prone to DNA rearrangements.

- read the PLoS ONE study
- see the press release
- check out U.S. News & World Report's take
- here's the Human Molecular Genetics abstract

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