Evidence map›Paper›PMID 42274578›Full record

ReviewCells2026

Autism Spectrum Disorder: Integrating Genetic and Environmental Risk.

Satoshi Kamijo, Hideki Miwa, Kazutaka Ikeda

Abstract readReview
In one paragraph

Review in Cells, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Satoshi KamijoDepartment of Neuropsychopharmacology, National Institute of Mental Health, National Center of Neurology and Psychiatry, Kodaira 187-8553, Tokyo, Japan.ORCID 0000-0002-4069-0742
Hideki MiwaDepartment of Neuropsychopharmacology, National Institute of Mental Health, National Center of Neurology and Psychiatry, Kodaira 187-8553, Tokyo, Japan.
Kazutaka IkedaDepartment of Neuropsychopharmacology, National Institute of Mental Health, National Center of Neurology and Psychiatry, Kodaira 187-8553, Tokyo, Japan.

Funding

Japan Society for the Promotion of Science JP22H04922 [AdAMS]Multilayered Stress Diseases, TMDU JPMXP1323015483
6 · The paper itself

Abstract

Autism spectrum disorder is a common neurodevelopmental condition, defined by persistent deficits in social interaction and communication, as well as restricted repetitive patterns of behavior, interests, or activities. Autism spectrum disorder is highly heterogeneous, encompassing a broad range of clinical presentations and suggesting it includes multiple etiological subtypes. Although no unified cause has been established, accumulating evidence indicates that genetic susceptibility interacts with environmental and developmental factors to shape diverse phenotypic outcomes. This review summarizes epidemiological findings and discusses major proposed etiological mechanisms, integrating evidence from human studies and animal models. Although animal models are not directly translatable to humans, their findings provide mechanistic insights that bridge epidemiological observations with neurobiological hypotheses.

Indexed as

Autism Spectrum DisorderEnvironmentGene-Environment InteractionGenetic Predisposition to DiseaseAnimalsHumansRisk Factorsautism spectrum disorder (ASD)brain–gut interactioncerebellumdopamineendocannabinoid systemexcitation/inhibition imbalanceGABAergic systemgenetic factorsmaternal immune activationoxytocinserotonin

Identifiers

PMID42274578
PMCPMC13256891

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.