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HLA-DQ – Maternal Immuno-Reactivity (Gluten Sensitivity) and Schizophrenia

2012, June Maternal Antibodies to Dietary Antigens and Risk for Nonaffective Psychosis in Offspring  Håkan Karlsson, Ph.D.; Åsa Blomström, M.D.; Susanne Wicks, Ph.D.; Shuojia Yang, M.Sc.; Robert H. Yolken, M.D.; Christina Dalman, M.D., Ph.D., American Journal of Psychiatry June 2012

2012, May Maternal gluten sensitivity linked to schizophrenia risk in children, Håkan Karlsson, Ph.D.; Åsa Blomström, M.D.; Susanne Wicks, Ph.D.; Shuojia Yang, M.Sc.; Robert H. Yolken, M.D.; Christina Dalman, M.D., Ph.D. Karolinska Institute and Johns Hopkins University, May 11, 2012 American Journal of psychiatry Online  Results: Levels of anti-gliadin IgG (but not anti-casein IgG) above the 90th percentile of levels observed among comparison subjects were associated with nonaffective psychosis (odds ratio=1.7, 95% CI=1.1–2.8). This association was not confounded by differences in maternal age, immigrant status, or mode of delivery. Similarly, gestational age at birth, ponderal index, and birth weight were not related to maternal levels of anti-gliadin IgG. Conclusion: High levels of anti-gliadin IgG in the maternal circulation are associated with an elevated risk for the development of a nonaffective psychosis in offspring. Research is needed to identify the mechanisms underlying this association in order to develop preventive strategies.

2012, April Maternal immune activation by poly(I:C) induces expression of cytokines IL-1β and IL-13, chemokine MCP-1 and colony stimulating factor VEGF in fetal mouse brain.[J Neuroinflammation. 2012. Arrode-Brusés GBrusés JL. Department of Anatomy and Cell Biology, The University of Kansas School of Medicine Conclusions: This study identified a significant increase in the concentration levels of the cytokines IL-1β and IL-13, the chemokine MCP-1 and the colony stimulating factor VEGF in the developing central nervous system during activation of an innate immune response, suggesting that these factors are mediators of the noxious effects of maternal immune activation on central nervous system development, with potential long-lasting effects on animal behavior.

2011, Dec. The nuclear factor-kB inhibitor pyrrolidine dithiocarbamate reduces polyinosinic-polycytidilic acid induced immune response in pregnant rats and teh behavioral defects of their adult offspring.  Song X, Li W, Yang Y, Zhao J, Jiang C, Li W, Lv L., Department of Psychiatry, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China. Behav Brain Funct. 2011 Dec

2011, Jan. The Immune System in Pregnancy: A Unique Complexity  Gil Mor, Ingrid Cardenas
Am J Reprod Immunol. Author manuscript; available in PMC 2011 January 24.
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2010, Sept. Novel Roles for Immune Molecules in Neural Development: Implications for Neurodevelopmental Disorders Paula A. Garay, A. Kimberley McAllister, Frontiers in Synaptic Neuroscience. 2010; 2: 136. Published online 2010 September 8  Abstract: Although the brain has classically been considered “immune-privileged”, current research suggests an extensive communication between the immune and nervous systems in both health and disease. Recent studies demonstrate that immune molecules are present at the right place and time to modulate the development and function of the healthy and diseased central nervous system (CNS). Indeed, immune molecules play integral roles in the CNS throughout neural development, including affecting neurogenesis, neuronal migration, axon guidance, synapse formation, activity-dependent refinement of circuits, and synaptic plasticity. Moreover, the roles of individual immune molecules in the nervous system may change over development. This review focuses on the effects of immune molecules on neuronal connections in the mammalian central nervous system – specifically the roles for MHCI and its receptors, complement, and cytokines on the function, refinement, and plasticity of geniculate, cortical and hippocampal synapses, and their relationship to neurodevelopmental disorders. These functions for immune molecules during neural development suggest that they could also mediate pathological responses to chronic elevations of cytokines in neurodevelopmental disorders, including autism spectrum disorders (ASD) and schizophrenia.
 
2009, Nov. Prenatal exposure to infection: a primary mechanism for abnormal dopaminergic development in schizophrenia Meyer U, Feldon J.  Laboratory of Behavioural Neurobiology, ETH Zurich, Schorenstrasse 16, Schwerzenbach 8603, Switzerland, Psychopharmacology (Berl). 2009 Nov  Conclusions: Dopaminergic mal-development in general, and following prenatal immune activation in particular, may represent a primary etiopathological mechanism in the development of schizophrenia and related disorders. This hypothesis differs from the view that dopaminergic abnormalities in schizophrenia may be secondary to abnormalities in other brain structures and/or neurotransmitter systems. The existence of primary dopaminergic mechanisms may have important implications for the identification and early treatment of individuals prodromally symptomatic for schizophrenia.
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2009, Jan. Activation of the maternal immune system alters cerebellar development in the offspring Shi L, Smith SE, Malkova N, Tse D, Su Y, Patterson PH., Biology Division, California Insititute of TEchnology, 391 S. Holliston Ave. Brain Behavior and Immunology, Jan. 2009

2005, June Towards an immuno-precipitated neurodevelopmental animal model of schizophrenia Meyer U, Feldon J., Schedlowski M. Yee BK, Laboratory of Behavioural Neurobiology, Swiss Federal Institute of Technology Zurich, Schorenstrasse 16, Schwerzenbach 8603, Switzerland, Neurosci Biobehav Rev. 2005;29(6

2004, May Elevated maternal interleukin-8 levels and risk of schizophrenia in adult offspring.  Brown ASHooton JSchaefer CAZhang HPetkova EBabulas VPerrin MGorman JMSusser ES. American Journal of Psychiatry, May, 2004 (research via Columbia University) Conclusion: Using prospectively collected prenatal sera in a large and well-characterized birth cohort, the authors have documented a significant association between maternal IL-8 level during the second trimester and risk of schizophrenia spectrum disorders in the offspring. These findings provide further support for a substantive role of in utero infection or inflammation in the etiology of schizophrenia. Moreover, these results may have important implications for elucidating the mechanisms by which disrupted fetal development raises the risk of this disorder.

2002  Human influenza viral infection in utero alters glial fibrillary acidic protein immunoreactivity in the developing brains of neonatal mice. Fatemi SH, Emamian ES, Sidwell RW, Kist DA, Stary JM, Earle JA, Thuras P. Mol Psychiatry. 2002;7(6):633-40.

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