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Schizophrenia Bulletin Advance Access originally published online on February 9, 2006
Schizophrenia Bulletin 2006 32(2):200-202; doi:10.1093/schbul/sbj052
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© The Author 2006. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org.

Prenatal Infection as a Risk Factor for Schizophrenia

Alan S Brown1,2
2 College of Physicians and Surgeons, Columbia University; New York State Psychiatric Institute, Columbia University, New York, NY; and Mailman School of Public Health, Columbia University, New York, NY

1To whom correspondence should be addressed; e-mail: asb11{at}columbia.edu.

Accumulating evidence suggests that prenatal exposure to infection contributes to the etiology of schizophrenia. This line of investigation has been advanced by birth cohort studies that utilize prospectively acquired data from serologic assays for infectious and immune biomarkers. These investigations have provided further support for this hypothesis and permitted the investigation of new infectious pathogens in relation to schizophrenia risk. Prenatal infections that have been associated with schizophrenia include rubella, influenza, and toxoplasmosis. Maternal cytokines, including interleukin-8, are also significantly increased in pregnancies giving rise to schizophrenia cases. Although replication of these findings is required, this body of work may ultimately have important implications for the prevention of schizophrenia, the elaboration of pathogenic mechanisms in this disorder, and investigations of gene-environment interactions.

Keywords: infection / virus / schizophrenia / prenatal / epidemiology


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