Evidence map›Paper›PMID 23999529›Full record

ArticleMolecular psychiatry2014

Common DNA methylation alterations in multiple brain regions in autism.

C Ladd-Acosta, K D Hansen, E Briem, M D Fallin, W E Kaufmann, A P Feinberg

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

Article in Molecular psychiatry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 205 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
205citing papers in PubMed, 4 pooled it
19.2field-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

205 citing papers in PubMed, 4 syntheses or guidelines pooled it, 337 citations in OpenAlex.

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  13. Microglia as critical mediators linking perinatal immune stress to mental health trajectories.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
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145 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

6 authors at 1 institution in 1 country.

C Ladd-Acosta1] Department of Epidemiology, Johns Hopkins School of Public Health, Baltimore, MD, USA [2] Center for Epigenetics, Institute for Basic Biomedical Science, Johns Hopkins School of Medicine, Baltimore, MD, USA.
K D Hansen1] Center for Epigenetics, Institute for Basic Biomedical Science, Johns Hopkins School of Medicine, Baltimore, MD, USA [2] Department of Biostatistics and Institute for Genetic Medicine, Johns Hopkins School of Public Health, Baltimore, MD, USA.
E Briem1] Center for Epigenetics, Institute for Basic Biomedical Science, Johns Hopkins School of Medicine, Baltimore, MD, USA [2] Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
M D Fallin1] Department of Epidemiology, Johns Hopkins School of Public Health, Baltimore, MD, USA [2] Center for Epigenetics, Institute for Basic Biomedical Science, Johns Hopkins School of Medicine, Baltimore, MD, USA.
W E KaufmannKennedy-Krieger Institute, Baltimore, MD, USA.
A P Feinberg1] Center for Epigenetics, Institute for Basic Biomedical Science, Johns Hopkins School of Medicine, Baltimore, MD, USA [2] Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Kennedy Krieger Institute · US

Funding

SYNAPTIC MECHANISMS IN HIPPOCAMPAL EPILEPTOGENESISP30HD018655 · NICHD · CHILDREN'S HOSPITAL BOSTON · PI POMEROY, SCOTT LOREN · 1985 to 2015
$26.2M
Minority Action PlanP50HG003233 · NHGRI · JOHNS HOPKINS UNIVERSITY · PI FEINBERG, ANDREW P. · 2004 to 2013
$22.4M
NHGRI NIH HHS 5P50HG003233NHGRI NIH HHS P50 HG003233NICHD NIH HHS P30 HD018655
6 · The paper itself

Abstract

Autism spectrum disorders (ASD) are increasingly common neurodevelopmental disorders defined clinically by a triad of features including impairment in social interaction, impairment in communication in social situations and restricted and repetitive patterns of behavior and interests, with considerable phenotypic heterogeneity among individuals. Although heritability estimates for ASD are high, conventional genetic-based efforts to identify genes involved in ASD have yielded only few reproducible candidate genes that account for only a small proportion of ASDs. There is mounting evidence to suggest environmental and epigenetic factors play a stronger role in the etiology of ASD than previously thought. To begin to understand the contribution of epigenetics to ASD, we have examined DNA methylation (DNAm) in a pilot study of postmortem brain tissue from 19 autism cases and 21 unrelated controls, among three brain regions including dorsolateral prefrontal cortex, temporal cortex and cerebellum. We measured over 485,000 CpG loci across a diverse set of functionally relevant genomic regions using the Infinium HumanMethylation450 BeadChip and identified four genome-wide significant differentially methylated regions (DMRs) using a bump hunting approach and a permutation-based multiple testing correction method. We replicated 3/4 DMRs identified in our genome-wide screen in a different set of samples and across different brain regions. The DMRs identified in this study represent suggestive evidence for commonly altered methylation sites in ASD and provide several promising new candidate genes.

Indexed as

Autistic DisorderCase-Control StudiesCerebellumDNA MethylationEpigenesis, GeneticFemaleGenetic Predisposition to DiseaseHumansMalePilot ProjectsPrefrontal CortexTemporal Lobe

Identifiers

PMID23999529
PMCPMC4184909
OpenAlexW2052689749

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.