Abstract
Abstract Overall Abstract: Modern genomic approaches have revealed that the structure of genetic predisposition to schizophrenia is incredibly complex. Translating this complexity into comprehensible neurobiology is a daunting challenge. I will present data from a collaborative effort that has taken a reductionist approach, studying the 22q11.2 microdeletion syndrome, a rare predisposition factor of large effect size. Using a mouse model of the microdeletion, we have defined a potentially causal chain of events leading from the microdeletion to deficits in working memory across multiple levels of analysis. I will then discuss whether and how the lessons learned from this neurobiological approach can be applied toward the much more challenging problem of common risk alleles of small effect size.
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