Evidence map›Paper›PMID 42288509›Full record

ArticleNature communications2026

Spatial architecture of autism pathogenesis reveals mosaic structural disarray during early development.

Li Lin, Tzuen Yih Saw, Nigel Chou, Jie Lin Jolene Goh, Jing Eugene Kwa, Wan Kee Chock, Vipul Singhal, Zheng Li, Mike J Huang, Huck Hui Ng and 5 more

Abstract read
In one paragraph

Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

15 authors.

Li LinBioinformatics Institute (BII), Agency for Science, Technology and Research (A*STAR), Singapore, Republic of Singapore.
Tzuen Yih SawGenome Institute of Singapore (GIS), Agency for Science Technology and Research (A*STAR), Singapore, Republic of Singapore.
Nigel ChouGenome Institute of Singapore (GIS), Agency for Science Technology and Research (A*STAR), Singapore, Republic of Singapore.
Jie Lin Jolene GohGenome Institute of Singapore (GIS), Agency for Science Technology and Research (A*STAR), Singapore, Republic of Singapore.
Jing Eugene KwaGenome Institute of Singapore (GIS), Agency for Science Technology and Research (A*STAR), Singapore, Republic of Singapore.
Wan Kee ChockGenome Institute of Singapore (GIS), Agency for Science Technology and Research (A*STAR), Singapore, Republic of Singapore.ORCID http://orcid.org/0000-0002-4851-484X
Vipul SinghalGenome Institute of Singapore (GIS), Agency for Science Technology and Research (A*STAR), Singapore, Republic of Singapore.ORCID http://orcid.org/0000-0003-1670-1824
Zheng LiGenome Institute of Singapore (GIS), Agency for Science Technology and Research (A*STAR), Singapore, Republic of Singapore.ORCID http://orcid.org/0000-0002-7060-2213
Mike J HuangGenome Institute of Singapore (GIS), Agency for Science Technology and Research (A*STAR), Singapore, Republic of Singapore.
Huck Hui NgGenome Institute of Singapore (GIS), Agency for Science Technology and Research (A*STAR), Singapore, Republic of Singapore.
Chiea Chuen KhorGenome Institute of Singapore (GIS), Agency for Science Technology and Research (A*STAR), Singapore, Republic of Singapore.ORCID http://orcid.org/0000-0002-1128-4729
Hwee Lee KuanBioinformatics Institute (BII), Agency for Science, Technology and Research (A*STAR), Singapore, Republic of Singapore.
Kok Hao ChenGenome Institute of Singapore (GIS), Agency for Science Technology and Research (A*STAR), Singapore, Republic of Singapore.
Shyam PrabhakarGenome Institute of Singapore (GIS), Agency for Science Technology and Research (A*STAR), Singapore, Republic of Singapore. prabhakars@a-star.edu.sg.
Jinyue LiuGenome Institute of Singapore (GIS), Agency for Science Technology and Research (A*STAR), Singapore, Republic of Singapore. liu_jinyue@a-star.edu.sg.ORCID http://orcid.org/0000-0003-2094-6365

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autism spectrum disorder (ASD) has been associated with diverse genetic factors and molecular changes. Yet, how pathophysiology emerges during development and contributes to clinical heterogeneity remains unclear. Here we use spatial and single-cell transcriptomics of genetically diverse patient-derived organoids of the prenatal cortex to map the spatial architecture of ASD pathogenesis. We find abnormal partitioning of progenitor and neuron zones alongside local patches of disorganized neurons that vary in distribution among patients. Such spatially mosaic disarray persists into neuronal maturation and is consistent with impaired adhesion between progenitors. Our findings suggest that the spatial landscape of biological processes leading to ASD may be more heterogeneous than previously thought. We propose a model in which different patterns of scattered abnormalities, arising from spatially mosaic pathogenesis during prenatal brain development, contribute to the wide range of symptoms and brain structure variations observed in ASD patients.

Indexed as

Autism Spectrum DisorderBrainMosaicismCerebral CortexFemaleHumansMaleNeurodevelopmentNeuronsOrganoidsSingle-Cell AnalysisSpatial Transcriptomics

Identifiers

PMID42288509
PMCPMC13408761

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.