Evidence map›Paper›PMID 32353336›Full record

ReviewTrends in neurosciences2020

Prenatal Origins of ASD: The When, What, and How of ASD Development.

Eric Courchesne, Vahid H Gazestani, Nathan E Lewis

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Trends in neurosciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
108citing papers in PubMed, 4 pooled it
35.9field-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

108 citing papers in PubMed, 4 syntheses or guidelines pooled it, 204 citations in OpenAlex.

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  9. Transcriptomic Convergence in Autism Spectrum Disorder: Synaptic, Immune-Glial and RNA-Regulatory Axes in the Human Cerebral Cortex.International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience · 2026
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48 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

3 authors at 2 institutions in 1 country.

Eric CourchesneDepartment of Neuroscience, University of California, San Diego, San Diego, CA 92093, USA; Autism Center of Excellence, University of California, San Diego, San Diego, CA 92037, USA. Electronic address: ecourchesne@ucsd.edu.
Vahid H GazestaniDepartment of Neuroscience, University of California, San Diego, San Diego, CA 92093, USA; Autism Center of Excellence, University of California, San Diego, San Diego, CA 92037, USA; Department of Pediatrics, University of California, San Diego, San Diego, CA 92093, USA.
Nathan E LewisDepartment of Pediatrics, University of California, San Diego, San Diego, CA 92093, USA; Department of Bioengineering, University of California, San Diego, San Diego, CA 92093, USA.
Center for Autism and Related Disorders · USUniversity of California, San Diego · US

Funding

Developmental Functional Genomics in ASD ToddlersR01MH110558 · NIMH · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI COURCHESNE, ERIC, LEWIS, NATHAN ENOCH · 2016 to 2020
$3.0M
Discovering Neural Biomarkers of Language and Social Development in ASD ToddlersR01DC016385 · NIDCD · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI COURCHESNE, ERIC, PIERCE, KAREN L · 2017 to 2021
$3.0M
NIDCD NIH HHS R01 DC016385NIMH NIH HHS R01 MH110558
6 · The paper itself

Abstract

Autism spectrum disorder (ASD) is a largely heritable, multistage prenatal disorder that impacts a child's ability to perceive and react to social information. Most ASD risk genes are expressed prenatally in many ASD-relevant brain regions and fall into two categories: broadly expressed regulatory genes that are expressed in the brain and other organs, and brain-specific genes. In trimesters one to three (Epoch-1), one set of broadly expressed (the majority) and brain-specific risk genes disrupts cell proliferation, neurogenesis, migration, and cell fate, while in trimester three and early postnatally (Epoch-2) another set (the majority being brain specific) disrupts neurite outgrowth, synaptogenesis, and the 'wiring' of the cortex. A proposed model is that upstream, highly interconnected regulatory ASD gene mutations disrupt transcriptional programs or signaling pathways resulting in dysregulation of downstream processes such as proliferation, neurogenesis, synaptogenesis, and neural activity. Dysregulation of signaling pathways is correlated with ASD social symptom severity. Since the majority of ASD risk genes are broadly expressed, many ASD individuals may benefit by being treated as having a broader medical disorder. An important future direction is the noninvasive study of ASD cell biology.

Indexed as

Autism Spectrum DisorderBrainCell DifferentiationFemaleHumansNeurogenesisNeuronal OutgrowthPregnancyautismbrain specificbroadly expressedgeneprenatalproliferationregulatorysynapse

Identifiers

PMID32353336
PMCPMC7373219
OpenAlexW3017304736

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.