Prenatal Poly(I:C) Exposure and Other Developmental Immune Activation Models in Rodent Systems
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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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MIA can be induced experimentally via immunogens such as polyinosinic-polycytidylic acid (poly(I:C)) and lipopolysaccharide (LPS).
“MIA can be induced experimentally via immunogens, such as polyinosinic-polycytidylic acid (poly(I:C)) and lipopolysaccharide (LPS).”
From Maternal immune activation dysregulation of the fetal brain transcriptome and relevance to the pathophysiology of autism spectrum disorder (2018) · cites this paper as [30]
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Aguilar‐Valles, A., Jung, S., Poole, S., Flores, C., & Luheshi, G. N. (2011) · Psychoneuroendocrinology · doi:10.1016/j.psyneuen.2011.11.003 · Cited by 45 · see citing works
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McGrath, J. J., & Richards, L. J. (2009) · Schizophrenia Bulletin · doi:10.1093/schbul/sbp004 · Cited by 40 · see citing works
Richtand, N. M., Ahlbrand, R. A., Horn, P. S., Stanford, K. E., Bronson, S. L., & McNamara, R. K. (2011) · Journal of Psychiatric Research · doi:10.1016/j.jpsychires.2011.02.007 · Cited by 38 · see citing works
Aguilar‐Valles, A., & Luheshi, G. N. (2010) · Psychoneuroendocrinology · doi:10.1016/j.psyneuen.2010.09.006 · Cited by 36 · see citing works
Animal Models of Schizophrenia and Related Disorders
(2011) · Neuromethods · doi:10.1007/978-1-61779-157-4 · Cited by 22 · see citing works
Brown, A. S. (2006) · American Journal of Psychiatry · doi:10.1176/appi.ajp.163.12.2178 · Cited by 22 · see citing works
Translational Neuroscience of Schizophrenia: Seeking a Meeting of Minds Between Mouse and Man
Kas, M. J., Kahn, R. S., Collier, D. A., Waddington, J. L., Ekelund, J., Porteous, D. J., Schughart, K., & Hovatta, I. (2011) · Science Translational Medicine · doi:10.1126/scitranslmed.3002917 · Cited by 20 · see citing works
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Maternal immune activation: Implications for neuropsychiatric disorders
Estes, M. L., & McAllister, A. K. (2016) · Science · doi:10.1126/science.aag3194 · Cited by 1,206 · see citing works
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Knuesel, I., Chicha, L., Britschgi, M., Schobel, S. A., Bodmer, M., Hellings, J. A., Toovey, S., & Prinssen, E. P. (2014) · Nature Reviews Neurology · doi:10.1038/nrneurol.2014.187 · Cited by 880 · see citing works
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DNA methylation analysis of the autistic brain reveals multiple dysregulated biological pathways
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Cortisol and Inflammatory Biomarkers Predict Poor Treatment Response in First Episode Psychosis
Mondelli, V., Ciufolini, S., Belvederi Murri, M., Bonaccorso, S., Di Forti, M., Giordano, A., Marques, T. R., Zunszain, P. A., Morgan, C., Murray, R. M., et al. (2015) · Schizophrenia Bulletin · doi:10.1093/schbul/sbv028 · Cited by 286 · see citing works
The future of rodent models in depression research
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The placental interleukin-6 signaling controls fetal brain development and behavior
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Goeden, N., Velasquez, J., Arnold, K. A., Chan, Y., Lund, B. T., Anderson, G. M., & Bonnin, A. (2016) · The Journal of Neuroscience · doi:10.1523/jneurosci.2534-15.2016 · Cited by 264 · see citing works
Tylee, D. S., Sun, J., Hess, J. L., Tahir, M. A., Sharma, E., Malik, R., Worrall, B. B., Levine, A. J., Martinson, J. J., Nejentsev, S., et al. (2018) · American Journal of Medical Genetics Part B: Neuropsychiatric Genetics · doi:10.1002/ajmg.b.32652 · Cited by 219 · see citing works
Mattei, D., Ivanov, A., Ferrai, C., Jordan, P., Guneykaya, D., Buonfiglioli, A., Schaafsma, W., Przanowski, P., Deuther-Conrad, W., Brust, P., et al. (2017) · Translational Psychiatry · doi:10.1038/tp.2017.80 · Cited by 222 · see citing works
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Weber-Stadlbauer, U., Richetto, J., Labouesse, M. A., Bohacek, J., Mansuy, I. M., & Meyer, U. (2017) · Molecular Psychiatry · doi:10.1038/mp.2016.41 · Cited by 170 · see citing works
Self-citationFever and sickness behavior: Friend or foe?
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Richetto, J., Massart, R., Weber-Stadlbauer, U., Szyf, M., Riva, M. A., & Meyer, U. (2017) · Biological Psychiatry · doi:10.1016/j.biopsych.2016.08.010 · Cited by 148 · see citing works
Self-citationLabouesse, M. A., Dong, E., Grayson, D. R., Guidotti, A., & Meyer, U. (2015) · Epigenetics · doi:10.1080/15592294.2015.1114202 · Cited by 138 · see citing works
Self-citationMadore, C., Leyrolle, Q., Lacabanne, C., Benmamar-Badel, A., Joffre, C., Nadjar, A., & Layé, S. (2016) · Neural Plasticity · doi:10.1155/2016/3597209 · Cited by 141 · see citing works
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Giovanoli, S., Notter, T., Richetto, J., Labouesse, M. A., Vuillermot, S., Riva, M. A., & Meyer, U. (2015) · Journal of Neuroinflammation · doi:10.1186/s12974-015-0437-y · Cited by 124 · see citing works
Self-citationBrunner, D., Kabitzke, P., He, D., Cox, K., Thiede, L., Hanania, T., Sabath, E., Alexandrov, V., Saxe, M., Peles, E., et al. (2015) · PLOS ONE · doi:10.1371/journal.pone.0134572 · Cited by 111 · see citing works
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da Silveira, V. T., de Castro Medeiros, D., Ropke, J., Guidine, P. A., Rezende, G. H., Moraes, M. F. D., Mendes, E. M. A. M., Macedo, D., Moreira, F. A., & de Oliveira, A. C. P. (2017) · International Journal of Developmental Neuroscience · doi:10.1016/j.ijdevneu.2017.01.009 · Cited by 51 · see citing works
The association between infections and general cognitive ability in young men – a nationwide study
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Between Dysbiosis, Maternal Immune Activation and Autism: Is There a Common Pathway?
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The Many Faces of Microbiota-Gut-Brain Axis in Autism Spectrum Disorder
Gonçalves, C. L., Doifode, T., Rezende, V. L., Costa, M. A., Rhoads, J. M., & Soutullo, C. A. (2024) · Life Sciences · doi:10.1016/j.lfs.2023.122357 · Cited by 42 · see citing works
- Authors
- Meyer, U.
- Affiliations
- ETH Zurich (CH)
- Corresponding author
- Meyer, Urs
- ORCID
- 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
- green
- zenodo.org
- Licence
- 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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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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