ABSTRACT
The cause(s) of schizophrenia remain elusive. While there is clear evidence that risk for schizophrenia can run in families and that genes playa role in risk for schizophrenia, the search for individual genes has been disappointing. The genes that have been identified confer only a small portion of overall risk. Against this backdrop, there has been renewed interest in perinatal environmental risk factors for schizophrenia. A large population-based study found that place of birth and season of birth accounted for 41.4% of the cases of schizophrenia based on population attributable risk, clearly demonstrating the importance of perinatal environmental factors in the etiology of schizophrenia. 1 The pathological mechanisms underlying prenatal and perinatal risk factors for schizophrenia remain largely unstudied. Understanding the mechanisms through which pre-and perinatal risk factors alter brain development will ultimately inform us about the underlying cellular and circuit pathology of schizophrenia, and provide strategies for preventing or mitigating risk. This chapter will review the evidence that suggests prenatal exposure to infection increases risk for schizophrenia, and consider mechanisms through which maternal infection could impact the developing fetal brain. Finally, it will focus on the role that inflammatory cytokines, generated by the maternal immune system in response to infection, play in altering fetal brain development and increasing risk for schizophrenia.
