Prenatal Infection as a Risk Factor for Schizophrenia

TLDR

Prenatal infections such as rubella, influenza, and toxoplasmosis, along with elevated maternal cytokines like interleukin‑8, are increasingly linked to schizophrenia risk. The study aims to replicate and extend evidence linking prenatal infections to schizophrenia, with implications for prevention, pathogenesis, and gene‑environment research. Birth cohort studies using prospectively collected serologic assays for infectious and immune biomarkers drive this research. These studies reinforce the infection hypothesis and enable exploration of additional pathogens linked to schizophrenia risk.

Abstract

Accumulating evidence suggests that prenatal exposure to infection contributes to the etiology of schizophrenia. This line of investigation has been advanced by birth cohort studies that utilize prospectively acquired data from serologic assays for infectious and immune biomarkers. These investigations have provided further support for this hypothesis and permitted the investigation of new infectious pathogens in relation to schizophrenia risk. Prenatal infections that have been associated with schizophrenia include rubella, influenza, and toxoplasmosis. Maternal cytokines, including interleukin-8, are also significantly increased in pregnancies giving rise to schizophrenia cases. Although replication of these findings is required, this body of work may ultimately have important implications for the prevention of schizophrenia, the elaboration of pathogenic mechanisms in this disorder, and investigations of gene-environment interactions.