Cited by 626Tryptophan and brain disordersNeuroinflammation and Neurodegeneration MechanismsStress Responses and Cortisol

Prenatal Poly(I:C) Exposure and Other Developmental Immune Activation Models in Rodent Systems

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Meyer, Urs·2014·Biological Psychiatry

Abstract

It is increasingly appreciated that altered neuroimmune mechanisms might play a role in the development of schizophrenia and related psychotic illnesses. On the basis of human epidemiological findings, a number of translational rodent models have been established to explore the consequences of prenatal immune activation on brain and behavioral development. The currently existing models are based on maternal gestational exposure to human influenza virus, the viral mimic polyriboinosinic-polyribocytidilic acid [Poly(I:C)], the bacterial endotoxin lipopolysaccharide, the locally acting inflammatory agent turpentine, or selected inflammatory cytokines. These models are pivotal for establishing causal relationships and for identifying cellular and molecular mechanisms that affect normal brain development in the event of early-life immune exposures. An important aspect of developmental immune activation models is that they allow a multi-faceted, longitudinal monitoring of the disease process as it unfolds during the course of neurodevelopment from prenatal to adult stages of life. An important recent refinement of these models is the incorporation of multiple etiologically relevant risk factors by combining prenatal immune challenges with specific genetic manipulations or additional environmental adversities. Converging findings from such recent experimental attempts suggest that prenatal infection can act as a "neurodevelopmental disease primer" that is likely relevant for a number of chronic mental illnesses. Hence, the adverse effects induced by prenatal infection might reflect an early entry into the neuropsychiatric route, but the specificity of subsequent disease or symptoms is likely to be strongly influenced by the genetic and environmental context in which the prenatal infectious process occurs.

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Crossref · 10.1016/j.biopsych.2013.07.011

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Authors
Meyer, U.
Affiliations
ETH Zurich (CH)
Corresponding author
Meyer, Urs
Venue
Biological Psychiatry
Publisher
Elsevier BV
Published
2014-02
Volume
75
Issue
4
Pages
307-315
ISSN
0006-3223 (ISSN-L)
OpenAlex
W2040408325
Cited by
626
References
104
Citations by year
2026: 30 · 2025: 37 · 2024: 49 · 2023: 48 · 2022: 61 · 2021: 54 · 2020: 47 · 2019: 59 · 2018: 58 · 2017: 49 · 2016: 58 · 2015: 43 · 2014: 27 · 2013: 3
FWCI
3.07
Type
journal article
Language
en
Open access
Locations
  • Biological Psychiatry (publishedVersion)
  • PubMed (publishedVersion)
  • Zenodo (CERN European Organization for Nuclear Research) (submittedVersion, other-oa)
Topics
  • Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
Keywords
prenatal immune activation, poly(I:C), rodent models, schizophrenia, neuroimmune mechanisms, brain development, maternal infection, lipopolysaccharide, turpentine, cytokines, genetic engineering, environmental adversity, chronic mental illness, prenatal infection
MeSH terms
Animals, Mental Disorders, Brain, Disease Models, Animal, Female, Humans, Inflammation, Poly I-C, Pregnancy, Pregnancy Complications, Infectious, Prenatal Exposure Delayed Effects, Rodentia, Virus Diseases, Maternal Exposure

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