NEW YORK (Reuters Health) - While a mother of an autistic child is pregnant, she develops an immune response to her fetus's brain. As part of that immune response, her body develops antibodies that can attack the fetal brain. Now, in new research in mice, scientists have discovered that the mother's fetal brain antibodies are circulated back to the fetus through the placenta, possibly triggering inflammation in the brain that could eventually result in autism.

At the Johns Hopkins Hospital in Baltimore, Maryland, Dr. Harvey Singer and colleagues took antibodies from human mothers of autistic children and injected them into pregnant mice, exposing the unborn mice pups to the antibodies as they circulated through the placenta. A second group of pregnant mice was injected with antibodies from mothers of non-autistic children. A third group of pregnant mice got no injections at all.

According to the researchers, autistic-like symptoms developed in the mice exposed before birth to the antibodies from the mothers of autistic children. For example, the affected mice behaved more anxiously, spent less time in open spaces, and were more hyperactive. They were also more easily startled by loud noises and were less social.

The differences between these mice and the pups that were not exposed prenatally to antibodies from mothers of autistic children became more pronounced as the animals moved from infancy to adulthood. As they aged, their autistic-like symptoms became more apparent. This pattern is also seen in humans with autism, who tend to develop new or more pronounced autistic symptoms over time.

"Comparing mice to humans is tricky," Singer cautioned in a prepared statement, "and we should be cautious anytime we do so, but our findings strongly suggest that the behaviors we observed in the offspring of mice injected with fetal brain antibodies from human mothers did behave in a manner that mimics some behaviors seen in people with autism."

"Autism is a complex disorder and it would be naïve to assume there's a single mechanism that can cause it," he said. "It's most likely the cumulative effect of several factors, including genes, metabolism, and the environment. We believe we have identified one of those factors."

SOURCE: Journal of Neuroimmunology, April 2009

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