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Published Online: 17 September 2018

Maternal Immune Activation and Neuropsychiatric Illness: A Translational Research Perspective

Abstract

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 Future
October 1857: The Pathology of Insanity
J.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)]

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Published In

Go to American Journal of Psychiatry
Go to American Journal of Psychiatry
American Journal of Psychiatry
Pages: 1073 - 1083
PubMed: 30220221

History

Received: 4 December 2017
Revision received: 18 April 2018
Accepted: 1 May 2018
Published online: 17 September 2018
Published in print: November 01, 2018

Keywords

  1. Epidemiology
  2. Neuropsychiatric Outcomes
  3. Animal Models
  4. Maternal Immune Activation
  5. Translation

Authors

Details

Alan S. Brown, M.D, M.P.H. [email protected]
From the New York State Psychiatric Institute, Columbia University Medical Center, New York; the Institute of Pharmacology and Toxicology, University of Zurich-Vetsuisse, Zurich; and the Neuroscience Center Zurich, University of Zurich and ETH Zurich.
Urs Meyer, Ph.D.
From the New York State Psychiatric Institute, Columbia University Medical Center, New York; the Institute of Pharmacology and Toxicology, University of Zurich-Vetsuisse, Zurich; and the Neuroscience Center Zurich, University of Zurich and ETH Zurich.

Notes

Address correspondence to Dr. Brown ([email protected]).

Funding Information

Swiss National Science Foundation: 310030_169544
National Institute of Environmental Health Sciences10.13039/100000066: 1R01ES019004

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