Evidence map›Paper›PMID 30094645›Full record

ReviewCurrent psychiatry reports2018

Prenatal Stress, Maternal Immune Dysregulation, and Their Association With Autism Spectrum Disorders.

David Q Beversdorf, Hanna E Stevens, Karen L Jones

Abstract readReview
In one paragraph

Review in Current psychiatry reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

51 citing papers in PubMed, 87 citations in OpenAlex.

  1. Gut microbes · 2026
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  8. Synergistic pathways to psychosis: understanding developmental risk and resilience factors.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
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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

3 authors at 3 institutions in 1 country.

David Q BeversdorfDepartments of Radiology, Neurology, and Psychological Sciences And The Thompson Center for Neurodevelopmental Disorders, University of Missouri, Columbia, MO, USA. beversdorfd@health.missouri.edu.
Hanna E StevensDepartments of Psychiatry and Pediatrics, Iowa Neuroscience Institute, University of Iowa, Iowa City, IA, USA.
Karen L JonesDepartment of Internal Medicine, Division of Rheumatology, Allergy, and Clinical Immunology, And the MIND Institute, University of California, Davis, Davis, CA, USA.
University of California, Davis · USUniversity of Iowa · USUniversity of Missouri · US

Funding

Pulmonary Toxicology Facility CoreP30ES005605 · NIEHS · UNIVERSITY OF IOWA · PI Brandi Janssen · 1990 to 2026
$40.5M
Research Training for Medical Students & Physician-Scientists in Child PsychiatryR25MH077823 · NIMH · YALE UNIVERSITY · PI ANDRES S MARTIN · 2006 to 2026
$4.0M
NIEHS NIH HHS P30 ES005605NIMH NIH HHS R25 MH077823
6 · The paper itself

Abstract

purpose of reviewWhile genetic factors are a major etiological contributor to autism spectrum disorder (ASD), evidence also supports a role for environmental factors. Herein, we will discuss two such factors that have been associated with a significant proportion of ASD risk: prenatal stress exposure and maternal immune dysregulation, and how sex and gender relate to these factors. RECENT

findingsRecent evidence suggests that maternal stress susceptibility interacts with prenatal stress exposure to affect offspring neurodevelopment. Additionally, understanding of the impact of maternal immune dysfunction on ASD has recently been advanced by recognition of specific fetal brain proteins targeted by maternal autoantibodies, and identification of unique mid-gestational maternal immune profiles. Animal models have been developed to explore pathophysiology targeting both of these factors, with limited sex-specific effects observed. While prenatal stress and maternal immune dysregulation are associated with ASD, most cases of these prenatal exposures do not result in ASD, suggesting interaction with multiple other risks. We are beginning to understand the behavioral, pharmacopathological, and epigenetic effects related to these interactions, as well as potential mitigating factors. Sex differences of these risks have been understudied but are crucial for understanding the higher prevalence of ASD in boys. Continued growth in understanding of these mechanisms may ultimately allow for the identification of multiple potential points for prevention or intervention, and for a personalized medicine approach for this subset of environmental-associated ASD cases.

Indexed as

AnimalsAutism Spectrum DisorderFemaleFetal ProteinsHumansPregnancyPregnancy ComplicationsPrenatal Exposure Delayed EffectsPrevalenceSex CharacteristicsStress, PsychologicalFetal ProteinsAntibodiesAutism spectrum disorderGene × environmentImmunityPrenatalStress

Identifiers

PMID30094645
PMCPMC6369590
OpenAlexW2885589494

What OpenQuestion holds

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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.