Some of the questions we try to answer are: What kind and how many different mutations increase the risk for schizophrenia? What kind of failures in neural circuits in our brain underlie these constellation of symptoms we refer to as schizophrenia? Why do neural circuits fail in particular ways and not others when our genetic program is disturbed by disease mutations? Why are conditions such as schizophrenia so frequent? Toward these goals, my laboratory has two interconnected research programs:
i. Genetics of Complex Psychiatric Disorders: Most psychiatric disorders have a strong genetic component and, therefore, our starting point is findings from human genetic approaches. Our genetics program has contributed a series of genetic discoveries especially on the contribution of rare mutations in the genetic architecture of schizophrenia.
ii. Animal Models of Complex Psychiatric Disorders: We are using mouse models of rare, recurrent, large-effect mutations to ask what are the consequences of a genetic lesion associated with mental illness in humans, on brain structure and function of a model organism, starting at the simpler cellular and synaptic levels to the higher-order circuit and behavior levels. Implementation of a range of state-of-the-art approaches to dissect the biological complexity of schizophrenia is the major component of my lab and has contributed a series of recent discoveries.
