Johns Hopkins researchers have genetically engineered the first mouse that models both the anatomical and behavioral defects of schizophrenia, a complex and debilitating brain disorder.
In contrast to current animal studies that rely on drugs that can only mimic the manifestations of schizophrenia, this new mouse is based on a genetic change relevant to the disease. Thus, it should greatly help with understanding disease progression and developing new therapies.
Animal models of schizophrenia have been hard to design since many different causes underlie this disease. However, Akira Sawa and colleagues took advantage of the recent discovery of a major risk factor for this disease: the DISC1 gene, which makes a protein that helps nerve cells assume their proper positions in the brain.
As reported online Monday in Proceedings of the National Academy of Sciences, the researchers generated mice that make an incomplete, shortened form of the DISC1 protein in addition to the regular type. The short form of the protein attaches to the full- length one, disrupting its normal duties.
As these mice matured, they became more agitated when placed in an open field, had trouble finding hidden food, and did not swim as long as regular mice; such behaviors parallel the hyperactivity, smell defects and apathy observed in schizophrenia patients. Magnetic resonance imaging also revealed characteristic defects in brain structure.
Sawa notes that the defects in these mice were not as severe as those typically seen in people with schizophrenia, because more than one gene is required to trigger the clinical disease.
"However, this mouse model will help us fill many gaps in schizophrenia research," he says. "We can use them to explore how external factors like stress or viruses may worsen symptoms. The animals can also be bred with other strains of genetically engineered mice to try to pinpoint additional schizophrenia genes. "
Source: Xinhua
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