INNOVATION:  Researchers at the University of California, Los Angeles have developed inducible dominant negative transgenic mice strains expressing different mutant DISC1 proteins. These mutations are thought to abolish the formation of normal DISC1 complexes by competing with endogenous DISC1 for available binding sites on target proteins. Researchers have found that the disruption of DISC1 protein during development produces deficits in sociability, latent inhibition and spatial working memory tasks in adult animals, thus effectively modeling the cognitive and social deficits associated with this disorder.

POTENTIAL APPLICATIONS:  Previous models of Schizophrenia attempt to mimic different aspects of this disorder by pharmacological means that do not reflect the etiology of the disorder. These mice are the first compelling genetic model of Schizophrenia and thus they could be used to better study the human phenotypes associated with DISC1 mutations and schizophrenia in general.

Reference: UCLA Case No. 2006-401