Traffic jam in brain causes
But new research from the Northwestern University Feinberg School of Medicine has revealed how schizophrenia works in the brain and provided a fresh opportunity for treatment. In a new, genetically engineered mouse model, scientists have discovered the disease symptoms are triggered by a low level of a brain protein necessary for neurons to talk to one another.
"Without enough pathways, the information takes much longer to travel between neurons and much of it will never arrive," said Peter Penzes, assistant professor of physiology at the Feinberg School. He is senior author of a paper reporting the findings published in a recent issue of the Proceedings of the National Academy of Science. Michael Cahill, a Feinberg doctoral student in neuroscience, is the lead author.
Currently the only drug treatment for schizophrenia is an antipsychotic. "The drugs address the hallucinations and calm down the patient, but they don't improve their working memory (the ability of the brain to temporarily store and manage information required for complex mental tasks such as learning and reasoning) or their ability to think or their social behavior," Penzes said. "So you end up with patients who still can't integrate into society. Many attempt suicide."
With the new mouse model, Penzes was able to demonstrate that the low level of kalirin resulted in fewer dendritic spines in the frontal cortex of the brain, the part of the brain responsible for problem solving, planning and reasoning. Other areas of the brain had a normal number of the dendritic spines. Human brains and mouse brains share many similarities in the way they function, Penzes said.
The new schizophrenic mouse model also exhibits more schizophrenic symptoms than other models, making these mice especially good for drug testing and development, Penzes said. The mice with low amounts of kalirin had a poor working memory, were antisocial and hyperactive.
Penzes said future studies would aim at enhancing the function of kalirin in the brain in an effort to correct the cognitive symptoms of schizophrenia.