ArticleMolecular autism2025
Exploring EEG resting state differences in autism: sparse findings from a large cohort.
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.
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Who cites it
8 citing papers in PubMed.
- The AHEPA EEG benchmark: setting the standard for machine learning in dementia diagnosis, a scoping review.Cognitive neurodynamics · 2026Article
- 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 · 2026Article
- Transdiagnostic EEG Signatures in ASD and ADHD: A Comparative Review of Computational Biomarkers and Neuromodulatory Interventions.Brain sciences · 2026Review
- Task-Related Aperiodic EEG (1/f) Activity in Autism.Autism research : official journal of the International Society for Autism Research · 2026Article
- Early Trajectories of Resting-State EEG power in autistic children: a longitudinal study across language profiles.Translational psychiatry · 2026Article
- Beta power as a neural correlate of sensory features in autistic individuals.Journal of neurodevelopmental disorders · 2026Article
- Conceptualizing the substrates and sequelae of decreased sound tolerance as a developmental cascade: A pilot study.Hearing research · 2026Article
- Explainable AI uncovers novel EEG microstate candidate neurophysiological markers for autism spectrum disorder.Frontiers in computational neuroscience · 2026Article
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
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.
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