The DOI matches its Crossref record; 86 of the 86 references it cites were found in a registry or an index.
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.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“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
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
From inflammation to sickness and depression: when the immune system subjugates the brain
Dantzer, R., O'Connor, J. C., Freund, G. G., Johnson, R. W., & Kelley, K. W. (2008) · Nature Reviews Neuroscience · doi:10.1038/nrn2297 · Cited by 7,395 · cited 1×
“In support of this, several cytokines seem to modulate processes of learning and memory, anxiety-related behaviors, and social interaction (3,78,79).”
Resolution of inflammation: the beginning programs the end
Serhan, C. N., & Savill, J. (2005) · Nature Immunology · doi:10.1038/ni1276 · Cited by 2,552 · cited 7×
“This idea of multiple hits with either sensitizing or preconditioning effects is also central to several theories of prenatal immune priming, which have been put forward by others in the context of peripheral immunity, CNS inflammation, perinatal brain damage, retinopathy, and various forms of learning and memory (68–…”
InfluentialA review of MRI findings in schizophrenia
Shenton, M. E., Dickey, C. C., Frumin, M., & McCarley, R. W. (2001) · Schizophrenia Research · doi:10.1016/s0920-9964(01)00163-3 · Cited by 2,346 · cited 1×
“One example is that autism has generally been associated with excessive brain growth (macrocephaly) involving thickening of cortex, increased gray and white matter, and lack of gray matter loss (41), whereas schizophrenia seems to be associated with microcephaly involving thinner cortical areas, reduced gray and white…”
Neuroglial activation and neuroinflammation in the brain of patients with autism
Vargas, D. L., Nascimbene, C., Krishnan, C., Zimmerman, A. W., & Pardo, C. A. (2005) · Annals of Neurology · doi:10.1002/ana.20315 · Cited by 2,149 · cited 1×
“For example, a nearly 50-fold increase in TNF- level was found in the cerebrospinal fluid (CSF) of autistic children (47), and severe inflammation is present in the brains of autistic patients from a broad range of ages (48), characterized by prominent activation of microglia and astroglia cells and enhanced proinflam…”
Schizophrenia genes, gene expression, and neuropathology: on the matter of their convergence
Harrison, P. J., & Weinberger, D. R. (2005) · Molecular Psychiatry · doi:10.1038/sj.mp.4001558 · Cited by 2,020 · cited 1×
“Such genetic components seem highly essential because both autism and schizophrenia exhibit strong patterns of heritability (83,84).”
Epidemiology of Pervasive Developmental Disorders
Fombonne, E. (2009) · Pediatric Research · doi:10.1203/pdr.0b013e31819e7203 · Cited by 1,971 · cited 1×
“In contrast to the delayed onset of schizophrenia, overt symptoms of autism often begin as early as by the age of 6 mo and become established by age 2 or 3 y (11,12).”
Microglial physiology: unique stimuli, specialized responses
Ransohoff, R. M., & Perry, V. H. (2009) · Annual Review of Immunology · doi:10.1146/annurev.immunol.021908.132528 · Cited by 1,858 · cited 3×
“In the CNS, microglia and astrocytes are the major immunocompetent cells, which regulate both the induction and limitation of inflammatory processes (45).”
Maternal Immune Activation Alters Fetal Brain Development through Interleukin-6
Smith, S. E. P., Li, J., Garbett, K., Mirnics, K., & Patterson, P. H. (2007) · The Journal of Neuroscience · doi:10.1523/jneurosci.2178-07.2007 · Cited by 1,605 · cited 1×
“The concept is further supported by the findings that blocking the actions of the proinflammatory cytokine IL-6 in the pregnant maternal host by genetic or pharmacological interventions prevents the long-term brain and behavioral consequences of prenatal PolyI:C treatment (39) and that over-expression of the antiinfla…”
Microglia in neurodegenerative disease
Perry, V. H., Nicoll, J. A. R., & Holmes, C. (2010) · Nature Reviews Neurology · doi:10.1038/nrneurol.2010.17 · Cited by 1,543 · cited 2×
“On the other hand, chronic or exaggerated microglial activation has been linked to multiple neuroinflammatory and neurodegenerative diseases, including Parkinson’s disease, multiple sclerosis, Alzheimer’s disease, and Huntington’s disease (46).”
Prenatal Infection and Schizophrenia: A Review of Epidemiologic and Translational Studies
Brown, A. S., & Derkits, E. J. (2010) · American Journal of Psychiatry · doi:10.1176/appi.ajp.2009.09030361 · Cited by 1,269 · cited 1×
“Epidemiologic studies suggest that the risk of schizophrenia is increased after prenatal maternal viral infections such as influenza, rubella, measles, and polio, as well as infections with bacterial pathogens and genital and/or reproductive infections (4).”
Cited by
Sorted by citations
Transcriptome-wide isoform-level dysregulation in ASD, schizophrenia, and bipolar disorder
Gandal, M. J., Zhang, P., Hadjimichael, E., Walker, R. L., Chen, C., Liu, S., Won, H., van Bakel, H., Varghese, M., Wang, Y., et al. (2018) · Science · doi:10.1126/science.aat8127 · Cited by 1,247
Maternal immune activation: Implications for neuropsychiatric disorders
Estes, M. L., & McAllister, A. K. (2016) · Science · doi:10.1126/science.aag3194 · Cited by 1,206
The role of inflammation in perinatal brain injury
Hagberg, H., Mallard, C. E., Ferriero, D. M., Vannucci, S. J., Levison, S. W., Vexler, Z. S., & Gressèns, P. (2015) · Nature Reviews Neurology · doi:10.1038/nrneurol.2015.13 · Cited by 852
Rook, G. A. (2013) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1313731110 · Cited by 760
Prenatal Poly(I:C) Exposure and Other Developmental Immune Activation Models in Rodent Systems
Meyer, U. (2014) · Biological Psychiatry · doi:10.1016/j.biopsych.2013.07.011 · Cited by 626
Self-citation
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
About these checks
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.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
