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Schizophrenia Bulletin Advance Access originally published online on April 11, 2008
Schizophrenia Bulletin 2009 35(5):959-972; doi:10.1093/schbul/sbn022
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© The Author 2008. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org.

A Review of the Fetal Brain Cytokine Imbalance Hypothesis of Schizophrenia

Urs Meyer, Joram Feldon1 and Benjamin K. Yee
Laboratory of Behavioural Neurobiology, ETH Zurich, Schorenstrasse 16, CH-8603 Schwerzenbach, Switzerland

1 To whom correspondence should be addressed; tel: +41 44 655 7448, fax: 41 44 655 7203, e-mail: feldon{at}behav.biol.ethz.ch.

Maternal infection during pregnancy increases the risk of schizophrenia and other brain disorders of neurodevelopmental origin in the offspring. A multitude of infectious agents seem to be involved in this association. Therefore, it has been proposed that factors common to the immune response to a wide variety of bacterial and viral pathogens may be the critical link between prenatal infection and postnatal brain and behavioral pathology. More specifically, it has been suggested that the maternal induction of pro-inflammatory cytokines may mediate the neurodevelopmental effects of maternal infections. Here, we review recent findings from in vitro and in vivo investigations supporting this hypothesis and further emphasize the influence of enhanced anti-inflammatory cytokine signaling on early brain development. Disruption of the fetal brain balance between pro- and anti-inflammatory cytokine signaling may thus represent a key mechanism involved in the precipitation of schizophrenia-related pathology following prenatal maternal infection and innate immune imbalances.

Keywords: animal model / cytokines / fetus / infection / neurodevelopment / pregnancy / schizophrenia


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