Evidence map›Paper›PMID 37508346›Full record

ArticleBiology2023

Autism Spectrum Disorder: A Neuro-Immunometabolic Hypothesis of the Developmental Origins.

Martin G Frasch, Byung-Jun Yoon, Dario Lucas Helbing, Gal Snir, Marta C Antonelli, Reinhard Bauer

Open access · goldAbstract read
In one paragraph

Article in Biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 2 pooled it
1.8field-weighted citation impact, top 15% 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

17 citing papers in PubMed, 2 syntheses or guidelines pooled it, 18 citations in OpenAlex.

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  14. Heart Rate Variability Code: Does It Exist and Can We Hack It?Bioengineering (Basel, Switzerland) · 2023
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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

6 authors at 5 institutions in 3 countries.

Martin G FraschDepartment of Obstetrics and Gynecology, University of Washington, Seattle, WA 98195, USA.ORCID 0000-0003-3159-6321
Byung-Jun YoonElectrical and Computer Engineering, Texas A&M University, College Station, TX 77843, USA.ORCID 0000-0001-9328-1101
Dario Lucas HelbingInstitute for Molecular Cell Biology, Jena University Hospital, Friedrich Schiller University, 07747 Jena, Germany.
Gal SnirDepartment of Obstetrics and Gynecology, University of Washington, Seattle, WA 98195, USA.
Marta C AntonelliInstituto de Biología Celular y Neurociencia "Prof. Eduardo De Robertis", Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires 1121, Argentina.
Reinhard BauerInstitute for Molecular Cell Biology, Jena University Hospital, Friedrich Schiller University, 07747 Jena, Germany.ORCID 0000-0002-4294-3758
University of Washington · USJena University Hospital · DELeibniz Institute on Aging - Fritz Lipmann Institute (FLI) · DETexas A&M University · USUniversidad de Buenos Aires · AR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fetal neuroinflammation and prenatal stress (PS) may contribute to lifelong neurological disabilities. Astrocytes and microglia, among the brain's non-neuronal "glia" cell populations, play a pivotal role in neurodevelopment and predisposition to and initiation of disease throughout lifespan. One of the most common neurodevelopmental disorders manifesting between 1-4 years of age is the autism spectrum disorder (ASD). A pathological glial-neuronal interplay is thought to increase the risk for clinical manifestation of ASD in at-risk children, but the mechanisms remain poorly understood, and integrative, multi-scale models are needed. We propose a model that integrates the data across the scales of physiological organization, from genome to phenotype, and provides a foundation to explain the disparate findings on the genomic level. We hypothesize that via gene-environment interactions, fetal neuroinflammation and PS may reprogram glial immunometabolic phenotypes that impact neurodevelopment and neurobehavior. Drawing on genomic data from the recently published series of ovine and rodent glial transcriptome analyses with fetuses exposed to neuroinflammation or PS, we conducted an analysis on the Simons Foundation Autism Research Initiative (SFARI) Gene database. We confirmed 21 gene hits. Using unsupervised statistical network analysis, we then identified six clusters of probable protein-protein interactions mapping onto the immunometabolic and stress response networks and epigenetic memory. These findings support our hypothesis. We discuss the implications for ASD etiology, early detection, and novel therapeutic approaches. We conclude with delineation of the next steps to verify our model on the individual gene level in an assumption-free manner. The proposed model is of interest for the multidisciplinary community of stakeholders engaged in ASD research, the development of novel pharmacological and non-pharmacological treatments, early prevention, and detection as well as for policy makers.

Indexed as

autism spectrum disordergenomicsinformation theorymulti-scale modeling

Identifiers

PMID37508346
PMCPMC10375982
OpenAlexW2972910442

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.