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Epidemiologic studies of exposure to prenatal infection and risk of schizophrenia and autism.
Dev Neurobiol 2012; 72(10):1272-6DN

Abstract

In this review, we provide a synopsis of work on the epidemiologic evidence for prenatal infection in the etiology of schizophrenia and autism. In birth cohort studies conducted by our group and others, in utero exposure to infectious agents, prospectively obtained after biomarker assays of archived maternal sera and by obstetric records was related to an increased risk of schizophrenia. Thus far, it has been demonstrated that prenatal exposure to influenza, increased toxoplasma antibody, genital-reproductive infections, rubella, and other pathogens are associated with schizophrenia. Anomalies of the immune system, including enhanced maternal cytokine levels, are also related to schizophrenia. Some evidence also suggests that maternal infection and immune dysfunction may be associated with autism. Although replication is required, these findings suggest that public health interventions targeting infectious exposures have the potential for preventing cases of schizophrenia and autism. Moreover, this work has stimulated translational research on the neurobiological and genetic determinants of these conditions.

Authors+Show Affiliations

College of Physicians and Surgeons of Columbia University, New York State Psychiatric Institute, New York, New York, USA. asb11@columbia.edu

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

22488761

Citation

Brown, Alan S.. "Epidemiologic Studies of Exposure to Prenatal Infection and Risk of Schizophrenia and Autism." Developmental Neurobiology, vol. 72, no. 10, 2012, pp. 1272-6.
Brown AS. Epidemiologic studies of exposure to prenatal infection and risk of schizophrenia and autism. Dev Neurobiol. 2012;72(10):1272-6.
Brown, A. S. (2012). Epidemiologic studies of exposure to prenatal infection and risk of schizophrenia and autism. Developmental Neurobiology, 72(10), pp. 1272-6. doi:10.1002/dneu.22024.
Brown AS. Epidemiologic Studies of Exposure to Prenatal Infection and Risk of Schizophrenia and Autism. Dev Neurobiol. 2012;72(10):1272-6. PubMed PMID: 22488761.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Epidemiologic studies of exposure to prenatal infection and risk of schizophrenia and autism. A1 - Brown,Alan S, Y1 - 2012/08/23/ PY - 2012/03/07/received PY - 2012/03/21/revised PY - 2012/03/23/accepted PY - 2012/4/11/entrez PY - 2012/4/11/pubmed PY - 2013/4/11/medline SP - 1272 EP - 6 JF - Developmental neurobiology JO - Dev Neurobiol VL - 72 IS - 10 N2 - In this review, we provide a synopsis of work on the epidemiologic evidence for prenatal infection in the etiology of schizophrenia and autism. In birth cohort studies conducted by our group and others, in utero exposure to infectious agents, prospectively obtained after biomarker assays of archived maternal sera and by obstetric records was related to an increased risk of schizophrenia. Thus far, it has been demonstrated that prenatal exposure to influenza, increased toxoplasma antibody, genital-reproductive infections, rubella, and other pathogens are associated with schizophrenia. Anomalies of the immune system, including enhanced maternal cytokine levels, are also related to schizophrenia. Some evidence also suggests that maternal infection and immune dysfunction may be associated with autism. Although replication is required, these findings suggest that public health interventions targeting infectious exposures have the potential for preventing cases of schizophrenia and autism. Moreover, this work has stimulated translational research on the neurobiological and genetic determinants of these conditions. SN - 1932-846X UR - https://www.unboundmedicine.com/medline/citation/22488761/Epidemiologic_studies_of_exposure_to_prenatal_infection_and_risk_of_schizophrenia_and_autism_ L2 - https://doi.org/10.1002/dneu.22024 DB - PRIME DP - Unbound Medicine ER -