Schizophrenia is a devastating psychiatric disease that affects 2-3 million individuals in the United States and approximately 1% of the population worldwide. It is characterized by "positive symptoms" such as delusions and hallucinations, "negative symptoms" including blunted emotions and social isolation, and cognitive deficits including impairments in attention and working memory. While currently available therapies for schizophrenia show effectiveness in some patients, many patients remain refractory to treatment and many more suffer significant side effects. In addition, treatments have historically been ineffective at treating its negative symptoms and cognitive impairments. Given the high incidence and severity of this illness and the lack of ideal therapies, there is a tremendous need for new treatments of schizophrenia.

Calcineurin is a serine/threonine protein phosphatase that is highly expressed in the mammalian brain and is involved in multiple neuronal functions. The laboratories of Dr. Susumu Tonegawa at MIT and Dr. Maria Karayiorgou at Rockefeller have obtained behavioral and genetic evidence indicating that calcineurin dysfunction contributes to schizophrenia pathogenesis. These findings raise the exciting possibility that the calcineurin pathway could be a novel and effective therapeutic target for this disease. We are leveraging our unique access to schizophrenia animal models and cutting-edge genomics-based research to better understand the role of calcineurin dysfunction in schizophrenia and to develop calcineurin-associated treatments for this debilitating disease. These animal models and human genetic resources further allow us to validate therapeutic targets and assess the efficacy of candidate compounds in an early stage of development.