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Does the brain become unglued in autism?
Date:12/11/2012

Philadelphia, PA, December 11, 2012 A new study published in Biological Psychiatry suggests that autism is associated with reductions in the level of cellular adhesion molecules in the blood, where they play a role in immune function.

Cell adhesion molecules are the glue that binds cells together in the body. Deficits in adhesion molecules would be expected to compromise processes at the interfaces between cells, influencing tissue integrity and cell-to-cell signaling. In the brain, deficits in adhesion molecules could compromise brain development and communication between nerve cells.

Over the years, deficits in neural cell adhesion molecules have been implicated in schizophrenia and other psychiatric disorders. One adhesion molecule, neurexin, is strongly implicated in the heritable risk for autism.

Cell adhesion molecules also play a crucial role in regulating immune cell access to the central nervous system. Prior research provided evidence of immune system dysfunction in individuals diagnosed with autism spectrum disorder (ASD). This led scientists from the University of California, Davis to examine whether adhesion molecules are altered in children with ASD.

To conduct the study, they recruited 2-4 year old children, 49 of whom were diagnosed with an ASD and 31 of whom were typically developing. They measured blood plasma levels of multiple molecules, conducted behavioral assessments, and measured head circumference in all participants.

"For the first time, we show that levels of soluble sPECAM-1 and sP-selectin, two molecules that mediate leukocyte migration, are significantly decreased in young children with ASD compared with typically developing controls of the same age," explained the authors. "This finding is consistent with previous reports of decreased levels of both sPECAM-1 and sP-selectin in adults with high-functioning autism."

They also found that repetitive behavior scores and sPEC
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Contact: Rhiannon Bugno
Biol.Psych@utsouthwestern.edu
214-648-0880
Elsevier
Source:Eurekalert

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