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Researchers learn more about genetic mutation linked to autism

f this missing DNA, certain proteins cannot form that normally contribute to glutamate synapses and, by extension, normal development.

"Now, using this information, we can look in a very detailed way at this gene in other families and begin to understand what happens when this protein that is normally active in the brain is missing," Wassink said.

Knowing more about how the deletions function could eventually lead to the development of diagnostic and therapeutic tools.


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Contact: Becky Soglin
becky-soglin@uiowa.edu
319-335-6660
University of Iowa
3-May-2007


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