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Disruption of Fetal Brain Development by Maternal Antibodies as an Etiological Factor in Schizophrenia

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Neural Development and Schizophrenia

Part of the book series: NATO ASI Series ((NSSA,volume 275))

Abstract

Various immunological abnormalities have been described in schizophrenics and in their family members. Usually these have been confined only to a subgroup of schizophrenics, and have been interpreted as evidence that some schizophrenia is caused by autoimmune processes occurring in postnatal life. However, recent discoveries indicate that the neuropathology of schizophrenia has a developmental basis, which is consistent with reports that maternal exposure to influenza in mid gestation increases the risk of subsequent schizophrenia in the offspring. The capability of influenza viruses to elicit autoimmune reactions to brain tissue in man and animals, and the proven causative role of maternal autoantibodies in various disease-states of the fetus and neonate, suggest a new interpretation of the immunological data: i.e. that the association of autoimmune phenomena with schizophrenia represents a familial manifestation of a maternal tendency to produce anti-brain autoantibodies which disrupt the development of the fetal brain. This view is supported by animal studies which demonstrate the teratogenic and behavioural effects of maternally administered anti-brain antibodies on the developing fetus.

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Laing, P., Knight, J.G., Wright, P., Irving, W.L. (1995). Disruption of Fetal Brain Development by Maternal Antibodies as an Etiological Factor in Schizophrenia. In: Mednick, S.A., Hollister, J.M. (eds) Neural Development and Schizophrenia. NATO ASI Series, vol 275. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1955-3_14

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