New findings show prenatal infection – a known risk factor for schizophrenia – can cause changes in the brain and behavior comparable to certain aspects of schizophrenia. The animal study shows that prenatal infection decreases functioning in key brain chemical receptors vital for long-term memory. The findings were presented at Neuroscience 2011, the annual meeting of the Society for Neuroscience and the world’s largest source of emerging news about brain science and health.
Schizophrenia is thought to reduce the function of proteins important in brain cell communication called N-methyl-D- aspartate receptors (NMDAR). The new study, led by Melissa Burt, at McGill University, suggests prenatal infection could lead to schizophrenia by decreasing NMDAR function.
To simulate prenatal infection, the researchers administered a bacterial toxin to pregnant rats. When the offspring reached adolescence, they showed reduced NMDAR function in the hippocampus, a brain structure important in memory. The animals also had deficits in spatial memory. People with schizophrenia often show memory deficits. “Understanding how specific environmental factors, like prenatal infection, increase the risk for schizophrenia is necessary in order to devise preventive strategies for this serious disorder,” Burt said.
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.
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Evidence supporting the hypothesis that prenatal infection plays a role in the etiology of schizophrenia is increasing. This article focuses on recent work from our group and others which has demonstrated that gestational exposure to influenza, other infections, and elevations of specific pro-inflammatory cytokines are associated with an increased risk of schizophrenia. In these investigations several methodological advantages have been brought to bear on informative birth cohorts and have helped to support and extend this hypothesis. These design advantages include prospective data using biomarkers on infection in maternal serum samples and direct assessment of cases.
The research was supported by the Canadian Institutes of Health Research.
Scientific Presentation: Wednesday, Nov. 16, 10 -11 a.m., Halls A -C
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Melissa Burt
McGill University Montreal,
Quebec
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Alan S Brown
College of Physicians and Surgeons, Columbia University; New York State Psychiatric Institute, Columbia University, New York, NY; and Mailman School of Public Health, Columbia University, New York, NY