Mice engineered to have smaller amounts of kalirin represent a better model for research, according to a study in PNAS.

Schizophrenia disease symptoms are triggered by a low level of a brain protein called kalirin, according to researchers from the Northwestern University Feinberg School of Medicine. Kalirin is needed to build the dense network of dendritic spines that allow information to flow from one neuron to another. Without an adequate amount, the frontal cortex of the brain of a person with schizophrenia only has a few narrow paths.

“Without enough pathways, the information takes much longer to travel between neurons, and much of it will never arrive,” says Peter Penzes, M.D., Ph.D., assistant professor of physiology at the Feinberg School. He is also the senior author of the paper, published in a recent issue of the Proceedings of the National Academy of Science, called “Kalirin regulates cortical spine morphogenesis and disease-related behavioral phenotypes.”

Previously in postmortem examinations of schizophrenic human brains, scientists found fewer connections between the brain cells in the frontal cortex and lower levels of kalirin. But they couldn’t show whether one condition led to the other.

Dr. Penzes thus developed a mouse model that had low levels of Kalirin. He was able to demonstrate that the low level of this protein resulted in fewer dendritic spines in the frontal cortex. Other areas of the brain had a normal number of the dendritic spines.

These mice also developed symptoms of schizophrenia at two months, equivalent to reaching adolescence in humans. This mimics the delayed onset of the disease in humans. In normal development, the brain ramps up the production of kalirin as it begins to mature in adolescence.

Additionally, the new schizophrenic mouse model also exhibited more symptoms than other models, Dr. Penzes states. They had a poor working memory and were antisocial and hyperactive.

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