![]() Most of the serological studies to date have come from 3 cohorts: 1) The Child Health and Development Studies (CHDS) cohort composed of all the births from 1959–1967 in Alameda County, California, 2) The Collaborative Perinatal Project (CPP) cohort comprised of multiple birth cohorts born between 19 based in different regions of the United States and 3) A Danish national birth cohort comprised of all pregnancies in that country since 1981. The cumulative results of both of these types of studies have been reviewed extensively elsewhere, so this review will focus primarily on results from cohorts with archived biological specimens. In some of these cohorts, infection verification came from analysis of medical records, while in others, infection status was determined serologically-either from archived maternal serum samples or from neonatal filter paper blood spots. ![]() To address some of the limitations of these ecological studies, subsequent epidemiological studies utilized population-based birth cohorts where data on infection status was available for each of the individual pregnancies. This type of misclassification is likely to have biased the results towards the null. In particular, misclassification of exposure was likely to occur because all offspring who were in utero during an epidemic were classified as `exposed' to infection, when in reality only a modest percentage of those mothers actually contracted influenza. Significant heterogeneity in the results from these studies may have reflected the difficulty of accurately classifying exposure status. However, the effect sizes for these associations were small and the findings were not consistently replicated. In Finnish, Danish and English populations, the occurrence of schizophrenia was higher among offspring in utero during influenza epidemics than among offspring in utero during comparable non-epidemic periods. Finally, directions for future research will be discussed.Įarly ecological studies identifying prenatal infection as a risk factor for schizophrenia used naturally occurring epidemics to query an association between in utero exposure to infection and later development of this psychiatric disorder (for review, see ). ![]() This review aims to summarize the major epidemiological and preclinical findings addressing the connection between prenatal infection and immune activation and later risk of developing schizophrenia, as well as the more limited literature addressing the mechanisms by which this gestational insult might affect offspring neurodevelopment. The findings from these preclinical studies indicate that severe infection and immune activation during pregnancy can negatively impact offspring brain development and impair adult behavior. ![]() These epidemiological studies inspired preclinical research using rodent and primate models of prenatal infection and MIA. A body of epidemiological literature has suggested an association between prenatal infection, subsequent maternal immune activation (MIA), and later risk of schizophrenia. Accordingly, many research studies relevant to schizophrenia have focused on understanding how genes or early environmental factors affect brain maturation. In recent decades it has become increasingly accepted that schizophrenia is a disorder of neurodevelopment.
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