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This article is more than five years old. Autism research - and science in general - is constantly evolving, so older articles may contain information or theories that have been reevaluated since their original publication date.
Sometimes, researchers can learn about a disorder by studying its opposite. That’s the strategy taken by Matthew Anderson, associate professor of pathology at Harvard University.
Anderson is interested in Angelman syndrome, which is characterized by developmental delay and a cheerful, social demeanor. The syndrome is caused by the loss of a gene called UBE3A. Intriguingly, some individuals with autism carry the reciprocal genetic glitch: duplications of UBE3A.
In October, Anderson created mice carrying duplications of the UBE3A gene. The animals show social and communicative problems and repetitive behaviors, all core characteristics of autism. On Tuesday, Anderson talked to SFARI.org about what these mice can teach us about autism.
For more reports from the 2011 Society for Neuroscience annual meeting, please click here.