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Prenatal infection and schizophrenia: a review of epidemiologic and translational studies.
Am J Psychiatry 2010; 167(3):261-80AJ

Abstract

An emerging literature from epidemiologic, clinical, and preclinical investigations has provided evidence that gestational exposure to infection contributes to the etiology of schizophrenia. In recent years, these studies have moved from ecologic designs, which ascertain infection based on epidemics in populations, to investigations that have capitalized on reliable biomarkers in individual pregnancies. These studies have documented specific candidate infections that appear to be associated with an elevated risk of schizophrenia. Animal models of maternal immune activation inspired by this work have revealed intriguing findings indicating behavioral, neurochemical, and neurophysiologic abnormalities consistent with observations in schizophrenia. In parallel studies in humans and animals, investigators are working to uncover the cellular and molecular mechanisms by which in utero exposure to infection contributes to schizophrenia risk. In this review, the authors discuss and critically evaluate the epidemiologic literature on in utero exposure to infection and schizophrenia, summarize emerging animal models of maternal immune activation, and discuss putative unique and common mechanisms by which in utero exposure to infection alters neurodevelopment, potentially increasing susceptibility to schizophrenia. The promise of this work for facilitating the identification of susceptibility loci in genetic studies of schizophrenia is illustrated by examples of interaction between in utero exposure to infection and genetic variants. The authors then elaborate on possible implications of this work, including the use of preventive measures for reducing the incidence of schizophrenia. Finally, they discuss new approaches aimed at addressing current challenges in this area of research.

Authors+Show Affiliations

New York State Psychiatric Institute, New York, NY 10032, USA. asb11@columbia.eduNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Review

Language

eng

PubMed ID

20123911

Citation

Brown, Alan S., and Elena J. Derkits. "Prenatal Infection and Schizophrenia: a Review of Epidemiologic and Translational Studies." The American Journal of Psychiatry, vol. 167, no. 3, 2010, pp. 261-80.
Brown AS, Derkits EJ. Prenatal infection and schizophrenia: a review of epidemiologic and translational studies. Am J Psychiatry. 2010;167(3):261-80.
Brown, A. S., & Derkits, E. J. (2010). Prenatal infection and schizophrenia: a review of epidemiologic and translational studies. The American Journal of Psychiatry, 167(3), pp. 261-80. doi:10.1176/appi.ajp.2009.09030361.
Brown AS, Derkits EJ. Prenatal Infection and Schizophrenia: a Review of Epidemiologic and Translational Studies. Am J Psychiatry. 2010;167(3):261-80. PubMed PMID: 20123911.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Prenatal infection and schizophrenia: a review of epidemiologic and translational studies. AU - Brown,Alan S, AU - Derkits,Elena J, Y1 - 2010/02/01/ PY - 2010/2/4/entrez PY - 2010/2/4/pubmed PY - 2010/3/23/medline SP - 261 EP - 80 JF - The American journal of psychiatry JO - Am J Psychiatry VL - 167 IS - 3 N2 - An emerging literature from epidemiologic, clinical, and preclinical investigations has provided evidence that gestational exposure to infection contributes to the etiology of schizophrenia. In recent years, these studies have moved from ecologic designs, which ascertain infection based on epidemics in populations, to investigations that have capitalized on reliable biomarkers in individual pregnancies. These studies have documented specific candidate infections that appear to be associated with an elevated risk of schizophrenia. Animal models of maternal immune activation inspired by this work have revealed intriguing findings indicating behavioral, neurochemical, and neurophysiologic abnormalities consistent with observations in schizophrenia. In parallel studies in humans and animals, investigators are working to uncover the cellular and molecular mechanisms by which in utero exposure to infection contributes to schizophrenia risk. In this review, the authors discuss and critically evaluate the epidemiologic literature on in utero exposure to infection and schizophrenia, summarize emerging animal models of maternal immune activation, and discuss putative unique and common mechanisms by which in utero exposure to infection alters neurodevelopment, potentially increasing susceptibility to schizophrenia. The promise of this work for facilitating the identification of susceptibility loci in genetic studies of schizophrenia is illustrated by examples of interaction between in utero exposure to infection and genetic variants. The authors then elaborate on possible implications of this work, including the use of preventive measures for reducing the incidence of schizophrenia. Finally, they discuss new approaches aimed at addressing current challenges in this area of research. SN - 1535-7228 UR - https://www.unboundmedicine.com/medline/citation/20123911/Prenatal_infection_and_schizophrenia:_a_review_of_epidemiologic_and_translational_studies_ L2 - https://ajp.psychiatryonline.org/doi/full/10.1176/appi.ajp.2009.09030361?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -