Projects:

Schizophrenia


Schizophrenia and cognition

Our laboratory has initiated a new research program to study the mechanism and develop treatments for the cognitive deficits associated with Schizophrenia. For that purpose we have derived and studied animal models with mutations, such as DISC1,  that are thought to cause the disorder in patients.  Our studies (for an example Click Here) show that a DISC1 inducible mutation causes cognitive, social, affective, and structural deficits in mice not unlike those seen in patients with DISC mutations. Amazingly, our studies demonstrated that this mutation only needs to be present for less than 24-hours during a critical period of post-natal development for all of these symptoms to be expressed. Thus, DISC1 mutant mice are helping us to understand this disorder, and may result in future treatments.

Key references

Ishizuka, K., Chen, J., Taya, S., Li, W., Millar, J.K., Xu, Y., Clapcote, S.J., Hookway, C., Morita, M., Kamiya, A., et al. (2007). Evidence that many of the DISC1 isoforms in C57BL/6J mice are also expressed in 129S6/SvEv mice. Molecular psychiatry 12, 897-899.

Li, W., Zhou, Y., Jentsch, J.D., Brown, R.A., Tian, X., Ehninger, D., Hennah, W., Peltonen, L., Lonnqvist, J., Huttunen, M.O Kaprio, J., Trachtenberg, J. T., Silva, A. J.*, Cannon, T. D.2007). Specific developmental disruption of disrupted-in-schizophrenia-1 function results in schizophrenia-related phenotypes in mice. Proc Natl Acad Sci U S A 104, 18280-18285. *corresponding author.(PDF)



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