Evidence map›Paper›PMID 17913903›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007

Maternal immune activation alters fetal brain development through interleukin-6.

Stephen E P Smith, Jennifer Li, Krassimira Garbett, Karoly Mirnics, Paul H Patterson

2 registry-linked trialsOpen access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 839 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
839citing papers in PubMed, 1 pooled it
15.5field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT01696929 phase1completednot on this mapstarted 2012, after this paper: background citation

An Open-Label Trial of Tocilizumab in Schizophrenia

TypeinterventionalSponsorBrian MillerRan2012 to 2014Enrolled8ConditionsSchizophreniaArmsTocilizumab
NCT02796859 phase1 / phase2unknown statusnot on this mapstarted 2016, after this paper: background citation

A Randomized Controlled Trial of Adjunctive Siltuximab in Schizophrenia

TypeinterventionalSponsorBrian MillerRan2016 to 2023Enrolled30ConditionsSchizophrenia, Psychotic DisordersArmsSiltuximab, normal saline
3 · Its place in the literature

Who cites it

839 citing papers in PubMed, 1 synthesis or guideline pooled it, 1,606 citations in OpenAlex.

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779 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Stephen E P SmithBiology Division, California Institute of Technology, Pasadena, California 91125, USA.
Jennifer Li
Krassimira Garbett
Karoly Mirnics
Paul H Patterson
California Institute of Technology · USJohn F. Kennedy Center for the Performing Arts · US

Funding

Maternal Viral Infection and Fetal Brain DevelopmentR01MH067978 · NIMH · CALIFORNIA INSTITUTE OF TECHNOLOGY · PI PATTERSON, PAUL H · 2004 to 2008
$1.6M
Autism Speaks AS1606NIMH NIH HHS R01 MH067978
6 · The paper itself

Abstract

Schizophrenia and autism are thought to result from the interaction between a susceptibility genotype and environmental risk factors. The offspring of women who experience infection while pregnant have an increased risk for these disorders. Maternal immune activation (MIA) in pregnant rodents produces offspring with abnormalities in behavior, histology, and gene expression that are reminiscent of schizophrenia and autism, making MIA a useful model of the disorders. However, the mechanism by which MIA causes long-term behavioral deficits in the offspring is unknown. Here we show that the cytokine interleukin-6 (IL-6) is critical for mediating the behavioral and transcriptional changes in the offspring. A single maternal injection of IL-6 on day 12.5 of mouse pregnancy causes prepulse inhibition (PPI) and latent inhibition (LI) deficits in the adult offspring. Moreover, coadministration of an anti-IL-6 antibody in the poly(I:C) model of MIA prevents the PPI, LI, and exploratory and social deficits caused by poly(I:C) and normalizes the associated changes in gene expression in the brains of adult offspring. Finally, MIA in IL-6 knock-out mice does not result in several of the behavioral changes seen in the offspring of wild-type mice after MIA. The identification of IL-6 as a key intermediary should aid in the molecular dissection of the pathways whereby MIA alters fetal brain development, which can shed new light on the pathophysiological mechanisms that predispose to schizophrenia and autism.

Indexed as

Maternal-Fetal RelationsAnalysis of VarianceAnimalsAntibodiesBehavior, AnimalBrainCytokinesEmbryo, MammalianEnzyme-Linked Immunosorbent AssayExploratory BehaviorFemaleFetal DevelopmentInterleukin-6Interpersonal RelationsLipopolysaccharidesMiceAntibodiesCytokinesInterleukin-6LipopolysaccharidesPoly I-C

Identifiers

PMID17913903
PMCPMC2387067
OpenAlexW2154965665

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.