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Engineered mouse mimics cognitive aspects of schizophrenia

circuits affected in people are more complex than the analogous circuits in rodents. In particular, the relative size of the prefrontal cortex that is involved in the cognitive deficits is much smaller in rodents than in primates. Some of the cognitive symptoms such as hallucinations or delusions are impossible to address.

"However, rodent models have the advantage of allowing direct tests of cause-effect relationships for specific aspects of the disease, such as some of the cognitive deficits," they concluded. "We here have been able to introduce genetically a single molecular alteration in a restricted and regulated fashion and to study its behavioral and physiological consequences."

The researchers said that their findings suggest that cognitive symptoms of schizophrenia may arise from subtle genetic differences in the dopamine receptor gene in schizophrenics that increase receptor activity.


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Source:Cell Press


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