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Study shows link between inflammation in maternal blood and schizophrenia in offspring.

Maternal inflammation as indicated by the presence in maternal blood of early gestational C-reactive protein, an established inflammatory biomarker, appears to be associated with greater risk for schizophrenia in offspring, according to researchers at Columbia University.

The Columbia researchers with colleagues in Finland conducted an analysis of data from the Finnish Prenatal Study of Schizophrenia, a large, national birth cohort with an extensive bio-bank. They tested for the presence of C-reactive protein in the maternal blood of 777 offspring with schizophrenia and compared the findings with those from 777 control subjects. Maternal C-reactive protein levels were assessed from archived maternal serum specimens.

They found that increasing maternal C-reactive protein levels were significantly associated with development of schizophrenia in offspring and remained significant after adjusting for potential confounders such as parental history of psychiatric disorders, twin/singleton birth, location of birth, and maternal socioeconomic status. For every 1 mg/L increase in maternal C-reactive protein, the risk of schizophrenia increased by 28%.

This is the first time that this association has been demonstrated, indicating that an infection or increased inflammation during pregnancy could increase the risk of schizophrenia in the offspring.  Inflammation has been shown to alter brain development in previous studies, and schizophrenia is a neurodevelopmental disorder. Thus, this study provides an important link between inflammation and schizophrenia and may help the medical community to better understand the biological mechanisms that lead to this disorder. To the extent that the increased inflammation is due to infection, this work may suggest that approaches aimed at preventing infection may have the potential to reduce risk of schizophrenia.  There are many other known causes of inflammation, including tissue injury and autoimmune disease, although the researchers did not examine these specific conditions in this study.

Source: Columbia University’s Mailman School of Public Health

Functional CRP pathways.  In response to cytokines such as IL-6 and IL-1β, hepatic expression of CRP increases dramatically. Circulating CRP opsonizes bacteria and apoptotic cells, facilitating their clearance via the complement system and FcγR-mediated phagocytosis. CRP ligation might contribute to the release by phagocytic cells of immunomodulatory cytokines such as IL-10. Evidence is mounting that plasma CRP deposited onto inflamed tissue breaks into biologically active monomeric subunits, to which have been attributed a range of proinflammatory effects. Abbreviations: CRP, C-reactive protein; LPC, lysophosphatidylcholine.  Vyse et al 2011.
Functional CRP pathways. In response to cytokines such as IL-6 and IL-1β, hepatic expression of CRP increases dramatically. Circulating CRP opsonizes bacteria and apoptotic cells, facilitating their clearance via the complement system and FcγR-mediated phagocytosis. CRP ligation might contribute to the release by phagocytic cells of immunomodulatory cytokines such as IL-10. Evidence is mounting that plasma CRP deposited onto inflamed tissue breaks into biologically active monomeric subunits, to which have been attributed a range of proinflammatory effects. Abbreviations: CRP, C-reactive protein; LPC, lysophosphatidylcholine. Vyse et al 2011.

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