An international team of researchers has confirmed that the malfunction of a gene causes schizophrenia and depression, according to a study published Thursday's issue of the journal Neuron.
The researchers said their findings in mice offer a possible animal model for developing treatments for schizophrenia and depression, which have been proven to share common genetic mechanisms by the researchers.
In their experiments, the researchers sought to explore the consequences of mutating a gene called "Disrupted in schizophrenia 1" (DISC1), which was found to be associated with schizophrenia, bipolar disorder and major depression.
The researchers' theory was that different mutant variations of DISC1 might have different pathological effects.
To test this theory, they screened a large population of mouse mutants to isolate two with different mutations in DISC1.
They found that, indeed, one of the mutant mouse strains exhibited abnormal behavior and memory deficiencies resembling the symptoms of schizophrenia in humans. Additionally, these symptoms could be alleviated in the mice by anti-psychotic drugs.
Similarly, the other mutant mouse strain showed behaviors that reflected depressive symptoms. These symptoms could be alleviated by an antidepressant, the researchers said.
Both types of DISC1 mutant mice exhibited the same kind of reduced brain volume seen in people with schizophrenia and depression, and both types showed biochemical abnormalities in the function of the protein produced by the DISC1 gene.
The researchers concluded that the different effects of anti-psychotic and antidepressant drugs on the two mutant strains "might provide clues to effective medications for these patient groups.
"Indeed, these mice could represent a model system to explore novel treatment and preventative strategies for certain symptoms of major mental illness."
They wrote that "our findings lend further credence to the growing recognition that schizophrenia and bipolar disorder share, at least in part, the common genetic etiologies and thus underlying molecular mechanisms".