Exposure to prenatal infection and risk of schizophrenia
- 1 Department of Psychiatry, Columbia University College of Physicians and Surgeons, New York State Psychiatric Institute, New York, NY, USA
- 2 Department of Epidemiology, Columbia University Mailman School of Public Health, New York, NY, USA
We provide a brief review of findings supporting a role for prenatal infection in the etiology of schizophrenia. Our group and others have conducted birth cohort studies to address whether in utero exposure to infectious agents, prospectively documented by biomarker assays of archived maternal sera, and by detailed obstetric records, confer an increased risk of schizophrenia in adult offspring. Prenatal exposure to influenza, elevated toxoplasma antibody, rubella, genital–reproductive infections, and other infections have been associated with an increased risk of schizophrenia among offspring. Animal models have supported these epidemiologic findings by revealing that maternal immune activation causes phenotypes analogous to those found in patients with schizophrenia. Given that exposure to microbial agents are preventable or treatable, they suggest that interventions to diminish the incidence of infection during pregnancy have the potential to prevent an appreciable proportion of schizophrenia cases. Given the clear genetic component to schizophrenia, future studies should include investigations of interactions between prenatal infection and susceptibility genes in the pathogenesis of schizophrenia.
Keywords: schizophrenia, infection, influenza, epidemiology, toxoplasmosis, rubella, birth cohort
Citation: Brown AS (2011) Exposure to prenatal infection and risk of schizophrenia. Front. Psychiatry 2:63. doi: 10.3389/fpsyt.2011.00063
Received: 17 June 2011;
Accepted: 02 November 2011;
Published online: 23 November 2011.
Edited by:Sulie L. Chang, Seton Hall University, USA
Reviewed by:Herb Lachman, Albert Einstein College of Medicine of Yeshiva University, USA
Mikhail Pletnikov, Johns Hopkins University, USA
Copyright: © 2011 Brown. This is an open-access article subject to a non-exclusive license between the authors and Frontiers Media SA, which permits use, distribution and reproduction in other forums, provided the original authors and source are credited and other Frontiers conditions are complied with.
*Correspondence: Alan S. Brown, New York State Psychiatric Institute, 1051 Riverside Drive, Unit 23, New York, NY 10032, USA. e-mail: email@example.com