Evidence map›Paper›PMID 37121464›Full record

ArticleNeurobiology of learning and memory2023

The intersection of genome, epigenome and social experience in autism spectrum disorder: Exploring modifiable pathways for intervention.

Lane Strathearn, Allison Momany, Emese Hc Kovács, William Guiler, Christine Ladd-Acosta

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

Article in Neurobiology of learning and memory, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

2 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Review
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

5 authors at 2 institutions in 1 country.

Lane StrathearnStead Family Department of Pediatrics, Carver College of Medicine, University of Iowa, 200 Hawkins Drive, Iowa City, IA 52242, USA; Department of Neuroscience and Pharmacology, Carver College of Medicine, University of Iowa, 51 Newton Road 2-471 Bowen Science Building, Iowa City, IA 52241, USA; Interdisciplinary Graduate Program in Neuroscience, University of Iowa, 356 Medical Research Center, Iowa City, IA 52242, USA; Center for Disabilities and Development, University of Iowa Stead Family Children's Hospital, 100 Hawkins Drive, Iowa City, IA 52242, USA; Hawkeye Intellectual and Developmental Disabilities Research Center (Hawk-IDDRC), University of Iowa, 100 Hawkins Drive, Iowa City, IA 52242, USA. Electronic address: lane-strathearn@uiowa.edu.
Allison MomanyStead Family Department of Pediatrics, Carver College of Medicine, University of Iowa, 200 Hawkins Drive, Iowa City, IA 52242, USA; Hawkeye Intellectual and Developmental Disabilities Research Center (Hawk-IDDRC), University of Iowa, 100 Hawkins Drive, Iowa City, IA 52242, USA. Electronic address: allison-momany@uiowa.edu.
Emese Hc KovácsDepartment of Neuroscience and Pharmacology, Carver College of Medicine, University of Iowa, 51 Newton Road 2-471 Bowen Science Building, Iowa City, IA 52241, USA. Electronic address: emese-chmielewski@uiowa.edu.
William GuilerInterdisciplinary Graduate Program in Neuroscience, University of Iowa, 356 Medical Research Center, Iowa City, IA 52242, USA. Electronic address: william-guiler@uiowa.edu.
Christine Ladd-AcostaDepartment of Epidemiology and the Wendy Klag Center for Autism and Developmental Disabilities, Bloomberg School of Public Health, Johns Hopkins University, 615 N. Wolfe Street, Baltimore, MD 21205, USA. Electronic address: claddac1@jhu.edu.
University of Iowa · USJohns Hopkins University · US

Funding

University of Iowa Hawkeye Intellectual and Developmental Disabilities Research Center (Hawk-IDDRC)P50HD103556 · NICHD · UNIVERSITY OF IOWA · PI EDWIN TED G. ABEL, Lane Strathearn · 2021 to 2026
$8.5M
NICHD NIH HHS P50 HD103556
6 · The paper itself

Abstract

The number of children diagnosed with autism spectrum disorder (ASD) has increased substantially over the past two decades. Current research suggests that both genetic and environmental risk factors are involved in the etiology of ASD. The goal of this paper is to examine how one specific environmental factor, early social experience, may be correlated with DNA methylation (DNAm) changes in genes associated with ASD. We present an innovative model which proposes that polygenic risk and changes in DNAm due to social experience may both contribute to the symptoms of ASD. Previous research on genetic and environmental factors implicated in the etiology of ASD will be reviewed, with an emphasis on the oxytocin receptor gene, which may be epigenetically altered by early social experience, and which plays a crucial role in social and cognitive development. Identifying an environmental risk factor for ASD (e.g., social experience) that could be modified via early intervention and which results in epigenetic (DNAm) changes, could transform our understanding of this condition, facilitate earlier identification of ASD, and guide early intervention efforts.

Indexed as

Autism Spectrum DisorderChildDNA MethylationEpigenesis, GeneticEpigenomeHumansOxytocinOxytocinAutism spectrum disorderDNA methylationEpigeneticsOxytocinOxytocin receptor geneSocial experience

Identifiers

PMID37121464
PMCPMC10330448
OpenAlexW4367310152

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.