Evidence map›Paper›PMID 39994801›Full record

ArticleMolecular autism2025

Exploring EEG resting state differences in autism: sparse findings from a large cohort.

Adam J O Dede, Wenyi Xiao, Nemanja Vaci, Michael X Cohen, Elizabeth Milne

Abstract read
In one paragraph

Article in Molecular autism, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. Article
  2. Cortical Network Overconnectivity Relates to Sensory, Cognitive, and Social Dimensions in Young Children With Autism Spectrum Disorder.Autism research : official journal of the International Society for Autism Research · 2026
    Article
  3. Review
  4. Task-Related Aperiodic EEG (1/f) Activity in Autism.Autism research : official journal of the International Society for Autism Research · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. 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

5 authors.

Adam J O DedeSchool of Psychology, University of Sheffield, Sheffield, S10 2TN, UK.
Wenyi XiaoSchool of Psychology, University of Sheffield, Sheffield, S10 2TN, UK.
Nemanja VaciSchool of Psychology, University of Sheffield, Sheffield, S10 2TN, UK.
Michael X CohenDonders Institute for Brain, Cognition and Behaviour, Radboud University, Nijmegen, 6525 EN, The Netherlands.
Elizabeth MilneSchool of Psychology, University of Sheffield, Sheffield, S10 2TN, UK. E.Milne@sheffield.ac.uk.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAutism is a complex neurodevelopmental condition, the precise neurobiological underpinnings of which remain elusive. Here, we focus on group differences in resting state EEG (rsEEG). Although many previous reports have pointed to differences between autistic and neurotypical participants in rsEEG, results have failed to replicate, sample sizes have typically been small, and only a small number of variables are reported in each study.

methodsHere, we combined five datasets to create a large sample of autistic and neurotypical individuals (n = 776) and extracted 726 variables from each participant's data. We computed effect sizes and split-half replication rate for group differences between autistic and neurotypical individuals for each EEG variable while accounting for age, sex and IQ. Bootstrapping analysis with different sample sizes was done to establish how effect size and replicability varied with sample size.

resultsDespite the broad and exploratory approach, very few EEG measures varied with autism diagnosis, and when larger effects were found, the majority were not replicable under split-half testing. In the bootstrap analysis, smaller sample sizes were associated with larger effect sizes but lower replication rates. LIMITATIONS: Although we extracted a comprehensive set of EEG signal components from the data, there is the possibility that measures more sensitive to group differences may exist outside the set that we tested. The combination of data from different laboratories may have obscured group differences. However, our harmonisation process was sufficient to reveal several expected maturational changes in the EEG (e.g. delta power reduction with age), providing reassurance regarding both the integrity of the data and the validity of our data-handling and analysis approaches.

conclusionsTaken together, these data do not produce compelling evidence for a clear neurobiological signature that can be identified in autism. Instead, our results are consistent with heterogeneity in autism, and caution against studies that use autism diagnosis alone as a method to categorise complex and varied neurobiological profiles.

Indexed as

Autistic DisorderElectroencephalographyRestAdolescentAdultChildCohort StudiesFemaleHumansMaleYoung AdultAutism diagnosisBig dataBiomarkersHeterogeneityNeurodevelopmental disordersNIMH data archiveReplicationResting state

Identifiers

PMID39994801
PMCPMC11853566

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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.