July 16, 2013
Brain Gene May Lead To Better Treatment For Schizophrenia And Depression
Rebekah Eliason for redOrbit.com - Your Universe Online
A new study involving brain impaired mice has the potential to improve therapy for people suffering from schizophrenia and major depressive disorder. While further research is necessary, this discovery is already being heralded as a major step toward understanding a variety of mental illnesses.The brain's prefrontal cortex, located in the anterior section of the frontal lobes, is associated with executive functions that help control and manage other cognitive processes like planning, problem solving and task switching. Together with colleagues, neuroscientist Alexander Johnson at Michigan State discovered a link between the prefrontal cortex, learning and behavioral deficits in mice possessing a gene connected with mental illness.
According to the Mayo Clinic: "Schizophrenia is a group of severe brain disorders in which people interpret reality abnormally. Schizophrenia may result in some combination of hallucinations, delusions, and disordered thinking and behavior.
"Contrary to some popular belief, schizophrenia isn't split personality or multiple personality. The word "schizophrenia" does mean 'split mind,' but it refers to a disruption of the usual balance of emotions and thinking."
Like many mental health disorders, schizophrenia is a chronic illness that generally requires lifelong treatment. Antipsychotic drugs are used to treat manifestations of schizophrenia such as hallucinations, but there is no significant treatment for other symptoms such as anhedonia, the inability to experience pleasure, or lack of motivation.
Johnson explained, "This study may well suggest that if we start targeting these brain-behavior mechanisms in people with mental illness, it may help to alleviate some of the cognitive and motivational symptoms, which to date remain largely untreated with current drug therapies."
Researchers experimented with two groups of mice. One group possessed a gene associated with mental illness and the second group was a healthy control group without the gene.
The first experiment was designed to test for cognitive abilities. Researchers presented mice with a tasty treat on one side of a conditioning box. After several feedings, the treat was moved to the opposite side of the box. Mice that had the gene for mental illness had greater difficulty readjusting to the treat being on the new side than the control group.
A second experiment tested the animals' motivation and required the mice to respond an increasing number of times each time they wanted to receive food. After three hours, all of the mice with the mental illness gene had simply given up and quit responding for food while only half of the control group had stopped responding.
Johnson explained the deficiencies may indicate problems in the prefrontal cortex area known as the orbitofrontal cortex. Continued research should include targeting this area.
The study was recently published in the journal Proceedings of the National Academy of Sciences.