Evidence map›Paper›PMID 30220221›Full record

ReviewThe American journal of psychiatry2018

Maternal Immune Activation and Neuropsychiatric Illness: A Translational Research Perspective.

Alan S Brown, Urs Meyer

Open access · greenAbstract readReview
In one paragraph

Review in The American journal of psychiatry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 152 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
152citing papers in PubMed, 1 pooled it
8.7field-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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

152 citing papers in PubMed, 1 synthesis or guideline pooled it, 292 citations in OpenAlex.

  1. Pooled it
  2. Maternal immune activation in mice recapitulates features of attention-deficit/hyperactivity disorder (ADHD) in susceptible offspring.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
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92 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

2 authors at 1 institution in 1 country.

Alan S BrownFrom the New York State Psychiatric Institute, Columbia University Medical Center, New York; the Institute of Pharmacology and Toxicology, University of Zurich-Vetsuisse, Zurich; and the Neuroscience Center Zurich, University of Zurich and ETH Zurich.
Urs MeyerFrom the New York State Psychiatric Institute, Columbia University Medical Center, New York; the Institute of Pharmacology and Toxicology, University of Zurich-Vetsuisse, Zurich; and the Neuroscience Center Zurich, University of Zurich and ETH Zurich.
University of Zurich · CH

Funding

Prenatal factors and risk of autism in a Finnish national birth cohortR01ES019004 · NIEHS · NEW YORK STATE PSYCHIATRIC INSTITUTE DBA RESEARCH FOUNDATION FOR MENTAL HYGIENE, INC · PI BROWN, ALAN STEWART · 2009 to 2017
$3.5M
Prenatal Factors in Autism and other Psychiatric Outcomes in a National Birth CohortR01ES028125 · NIEHS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI BROWN, ALAN STEWART · 2017 to 2021
$2.3M
NIEHS NIH HHS R01 ES019004NIEHS NIH HHS R01 ES028125
6 · The paper itself

Abstract

Epidemiologic studies, including prospective birth cohort investigations, have implicated maternal immune activation in the etiology of neuropsychiatric disorders. Maternal infectious pathogens and inflammation are plausible risk factors for these outcomes and have been associated with schizophrenia, autism spectrum disorder, and bipolar disorder. Concurrent with epidemiologic research are animal models of prenatal immune activation, which have documented behavioral, neurochemical, neuroanatomic, and neurophysiologic disruptions that mirror phenotypes observed in these neuropsychiatric disorders. Epidemiologic studies of maternal immune activation offer the advantage of directly evaluating human populations but are limited in their ability to uncover pathogenic mechanisms. Animal models, on the other hand, are limited in their generalizability to psychiatric disorders but have made significant strides toward discovering causal relationships and biological pathways between maternal immune activation and neuropsychiatric phenotypes. Incorporating these risk factors in reverse translational animal models of maternal immune activation has yielded a wealth of data supporting the predictive potential of epidemiologic studies. To further enhance the translatability between epidemiology and basic science, the authors propose a complementary approach that includes deconstructing neuropsychiatric outcomes of maternal immune activation into key pathophysiologically defined phenotypes that are identifiable in humans and animals and that evaluate the interspecies concordance regarding interactions between maternal immune activation and genetic and epigenetic factors, including processes involving intergenerational disease transmission. [AJP AT 175: Remembering Our Past As We Envision Our Future October 1857: The Pathology of Insanity J.C. Bucknill: "In the brain the state of inflammation itself either very quickly ceases or very soon causes death; but when it does cease it leaves behind it consequences which are frequently the causes of insanity, and the conditions of cerebral atrophy." (Am J Psychiatry 1857; 14:172-193 )].

Indexed as

AnimalsAutistic DisorderBipolar DisorderChildFemaleHumansNeurodevelopmental DisordersPregnancyPregnancy ComplicationsPregnancy Complications, InfectiousSchizophreniaTranslational Research, BiomedicalAnimal ModelsEpidemiologyMaternal Immune ActivationNeuropsychiatric OutcomesTranslation

Identifiers

PMID30220221
PMCPMC6408273
OpenAlexW2890708734

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.