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 [which was pioneered by the good people at johns hopkins], scientists have discovered the disease symptoms are triggered by a low level of a brain protein necessary for neurons to talk to one another.
in human and mouse brains, kalirin [named after the multiple-handed hindu goddess kali for its ability to interact with numerous other proteins] is the brain protein needed to build the dense network of highways, called dendritic spines, which allow information to flow from one neuron to another. northwestern scientists have found that without adequate kalirin, the frontal cortex of the brain of a person with schizophrenia only has a few narrow roads. the information from neurons gets jammed up like rush hour traffic on an interstate highway squeezed to a single lane.
“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.
“this discovery opens a new direction for treating the devastating cognitive symptoms of schizophrenia,” penzes said. “there is currently no treatment for that. it suggests that if you can stimulate and amplify the activity of the protein kalirin that remains in the brain, perhaps we can help the symptoms.”
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.”
here is a study on the effect of the use of antipsychotics, particularly clozapine, by people with schizophrenia.
the following is an excerpt from an article which reviews the literature on suicide and suicide prevention of people with schizophrenia, where the suicide rate is anywhere from 5% to 29%:
mann et al.  reviewed the literature and identified a number of strategies that are effective in the prevention of suicide such as education and awareness programs for the general public, primary care providers and other gatekeepers, screening for individuals at high risk, and providing treatment using pharmacotherapy and psychotherapy. in particular, the prevention of suicide in schizophrenia should include providing proper information for the family members of the patient in the hope of reducing their hostility toward the patient. in addition, continuity of care after suicide attempts, restricting access to lethal methods and media reporting guidelines are important strategies to prevent suicide. since it is such a strong predictor of future suicide, preventing and reducing attempted suicide in schizophrenia may have a positive long-term impact.