Prenatal Infection and Schizophrenia: A Review of Epidemiologic and Translational Studies
By Alan S. Brown, Elena Derkits. American Journal of Psychiatry, 2010
1,244 citations recorded by the source corpus.
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.
Subfields: Biological Psychiatry, Immunology, Social Psychology
View Paper: https://www.semanticscholar.org/paper/f4e920e5be5d16f1e045d3e5931979b690a2f09b
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Citations in the corpus
- The Adverse Effects of Air Pollution on the Nervous System (2012, background): “Schizophrenia is caused through a combination of genetic factors and environmental insults, for instance prenatal infection [131].”
- Are we facing a crashing wave of neuropsychiatric sequelae of COVID-19? Neuropsychiatric symptoms and potential immunologic mechanisms (2020, neutral): “Exposure to viral infections in utero, during childhood development, and in adulthood have each been associated with increased risk of developing schizophrenia (Brown and Derkits, 2010; Khandaker et al., 2012; Menninger, 1926).”
- Animal models of schizophrenia (2011, background): “For instance, maternal exposure to either bacterial or viral infection during pregnancy elevates circulatory pro-inflammatory cytokines and other mediators of inflammation, affects brain development in the offspring and is associated with an increased risk of schizophrenia (Brown and Derkits, 2010; ”
- Effects of prenatal infection on brain development and behavior: a review of findings from animal models. (2010, positive): “An extensive literature has described that increased risk for schizophrenia is associated with a history of prenatal infection with a wide variety of different infectious agents (reviewed by Brown and Derkits, 2010).”
- Maternal immune activation yields offspring displaying mouse versions of the three core symptoms of autism (2012, background): “This is not surprising, as maternal infection is a well-characterized risk factor for schizophrenia as well as autism (Brown and Derkits, 2010).”