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Maternal Immune Activation and Neuropsychiatric Illness: A Translational Research Perspective

The American journal of psychiatry, 2018-11, Vol.175 (11), p.1073-1083 [Peer Reviewed Journal]

Copyright © 2018 by the American Psychiatric Association 2018 ;Copyright American Psychiatric Association Nov 1, 2018 ;ISSN: 0002-953X ;EISSN: 1535-7228 ;DOI: 10.1176/appi.ajp.2018.17121311 ;PMID: 30220221

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  • Title:
    Maternal Immune Activation and Neuropsychiatric Illness: A Translational Research Perspective
  • Author: Brown, Alan S ; Meyer, Urs
  • Subjects: Animals ; Autistic Disorder - immunology ; Behavior disorders ; Bipolar Disorder - immunology ; Child ; Epidemiology ; Epigenetics ; Female ; Humans ; Immune system ; Maternal & child health ; Neurodevelopmental Disorders - immunology ; Neuropsychology ; Pregnancy ; Pregnancy Complications - epidemiology ; Pregnancy Complications - immunology ; Pregnancy Complications, Infectious - epidemiology ; Pregnancy Complications, Infectious - immunology ; Schizophrenia - immunology ; Translational Medical Research
  • Is Part Of: The American journal of psychiatry, 2018-11, Vol.175 (11), p.1073-1083
  • Description: Epidemiologic studies, including prospective birth cohort investigations, have implicated maternal immune activation in the etiology of neuropsychiatric disorders. Maternal infectious pathogens and inflammation are plausible risk factors for these outcomes and have been associated with schizophrenia, autism spectrum disorder, and bipolar disorder. Concurrent with epidemiologic research are animal models of prenatal immune activation, which have documented behavioral, neurochemical, neuroanatomic, and neurophysiologic disruptions that mirror phenotypes observed in these neuropsychiatric disorders. Epidemiologic studies of maternal immune activation offer the advantage of directly evaluating human populations but are limited in their ability to uncover pathogenic mechanisms. Animal models, on the other hand, are limited in their generalizability to psychiatric disorders but have made significant strides toward discovering causal relationships and biological pathways between maternal immune activation and neuropsychiatric phenotypes. Incorporating these risk factors in reverse translational animal models of maternal immune activation has yielded a wealth of data supporting the predictive potential of epidemiologic studies. To further enhance the translatability between epidemiology and basic science, the authors propose a complementary approach that includes deconstructing neuropsychiatric outcomes of maternal immune activation into key pathophysiologically defined phenotypes that are identifiable in humans and animals and that evaluate the interspecies concordance regarding interactions between maternal immune activation and genetic and epigenetic factors, including processes involving intergenerational disease transmission.[AJP AT 175: Remembering Our Past As We Envision Our FutureOctober 1857: The Pathology of InsanityJ.C. Bucknill: “In the brain the state of inflammation itself either very quickly ceases or very soon causes death; but when it does cease it leaves behind it consequences which are frequently the causes of insanity, and the conditions of cerebral atrophy.” (Am J Psychiatry 1857; 14:172–193)]
  • Publisher: United States: American Psychiatric Association
  • Language: English
  • Identifier: ISSN: 0002-953X
    EISSN: 1535-7228
    DOI: 10.1176/appi.ajp.2018.17121311
    PMID: 30220221
  • Source: MEDLINE
    Alma/SFX Local Collection
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