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Schizophrenia and Autism: Both Shared and Disorder-Specific Pathogenesis Via Perinatal Inflammation?
Open accessAbstract
Prenatal exposure to infection and subsequent inflammatory responses have been implicated in the etiology of schizophrenia and autism. In this review, we summarize current evidence from human and animal studies supporting the hypothesis that the pathogenesis of these two disorders is linked via exposure to inflammation at early stages of development. Moreover, we propose a hypothetical model in which inflammatory mechanisms may account for multiple shared and disorder-specific pathological characteristics of both entities. In essence, our model suggests that acute neuroinflammation during early fetal development may be relevant for the induction of psychopathological and neuropathological features shared by schizophrenia and autism, whereas postacute latent and persistent inflammation may contribute to schizophrenia- and autism-specific phenotypes, respectively.
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“Multiple animal models of prenatal infection have found evidence of diverse neurobehavioral abnormalities, whether through direct exposure of pregnant mice or rodents to influenza virus, or through non-infectious activation of the maternal immune system (e.g., using RNA poly(I:C) to stimulate an antiviral inflammatory response or lipopolysaccharide to stimulate a bacterial inflammatory response) (”
From Maternal hospitalization with infection during pregnancy and risk of autism spectrum disorders (2015) · cites this paper as Meyer et al., 2011
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From inflammation to sickness and depression: when the immune system subjugates the brain
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InfluentialA review of MRI findings in schizophrenia
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Metadata
- Authors
- MEYER, U., FELDON, J., & DAMMANN, O.
- Affiliations
- ETH Zurich (CH)
- Tufts Medical Center (US)
- Corresponding author
- MEYER, URS
- Venue
- Pediatric Research
- Published
- 2011-05
- Volume
- 69
- Issue
- 5 Part 2
- Pages
- 26R-33R
- ISSN
- 0031-3998 (ISSN-L)
- PMC
- PMC3086802
- OpenAlex
- W2011183628
- Cited by
- 357
- References
- 86
- Citations by year
- 2026: 7 · 2025: 7 · 2024: 14 · 2023: 20 · 2022: 13 · 2021: 18 · 2020: 19 · 2019: 22 · 2018: 30 · 2017: 31 · 2016: 30 · 2015: 36 · 2014: 32 · 2013: 32 · 2012: 30
- FWCI
- 1.83
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Pediatric Research (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Science Foundation
- National Alliance for Research on Schizophrenia and Depression
- European Commission (LSHM‐CT‐2006‐036534, 241778)
- Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (116719, 100309)
- Eidgenössische Technische Hochschule Zürich (11 07/03)
- National Institutes of Health
- National Eye Institute (R21EY019253)
- Topics
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
- Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
- Keywords
- schizophrenia, autism spectrum disorder, perinatal inflammation, prenatal infection, neuroinflammation, fetal development, shared pathogenesis, chronic inflammation, psychopathology, neuropathology
- MeSH terms
- Autistic Disorder, Female, Humans, Inflammation, Models, Theoretical, Pregnancy, Pregnancy Complications, Schizophrenia
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