Gene clue for autism in mice4th May 2006
In findings published in the Neuron, scientists at the University of Texas have created "autistic" mice by deleting a single gene in key parts of the brain. US researchers found the mice had traits such as poor social interaction and high sensitivity. This could point the way to better understanding of the causes of autism, the researchers say.
Autistic spectrum disorders tend to emerge in childhood, and affect about 90 in 10,000 people, with boys tending to be affected more often than girls.
The University of Texas team looked at mice where the Pten gene, already linked to other brain disorders, was deleted in the mature nerve cells in the cerebral cortex and hippocampus areas of the brain, which are associated with higher brain function such as learning and memory.
The mice behaved in a number of socially abnormal ways, say the researchers, compared to another group of mice from the same litter; they were socially less skilled, being far less likely to be curious about new animals coming into the cage.
The mice mirrored the type behaviour of children with autistic spectrum disorders, for example by showing the same level of interest in an empty cage and in one containing another mouse. The genetically altered mice were also less likely to build nests or look after their young, but were more sensitive to stressful stimuli, such as loud noises or being picked up. They had the increased brain volume and enlarged heads seen in people with autistic spectrum disorders.
Anthony Wynshaw-Boris and Joy Greer from the University of California San Diego School of Medicine in La Jolla said the findings are 'intriguing', but they caution that the research does not provide the complete answer; there were other behaviours seen in people with autistic spectrum disorders, for example repetitive behaviours, which were not seen in the mice.
Professor Simon Baron Cohen, of the Autism Research Centre in Cambridge, said that the research 'may have some relevance to understanding the genetic basis of autism spectrum conditions'. He added that social abnormalities in a mouse may be caused by very different factors to human social abnormalities.
He cautioned that further human, clinical studies will be needed to test if PTEN is a susceptibility gene for autistic spectrum disorders. He added, however, that this new study added to the understanding of how genes expressed in the brain may have specific functions related to neuroanatomy and behaviour.
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