Evidence map›Paper›PMID 25538564›Full record

ReviewFrontiers in cellular neuroscience2014

Convergence of circuit dysfunction in ASD: a common bridge between diverse genetic and environmental risk factors and common clinical electrophysiology.

Russell G Port, Michael J Gandal, Timothy P L Roberts, Steven J Siegel, Gregory C Carlson

Abstract readReview
In one paragraph

Review in Frontiers in cellular neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing 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

22 citing papers in PubMed.

  1. Article
  2. bioRxiv : the preprint server for biology · 2025
    Article
  3. Parsing evoked and induced gamma response differences in Autism: A visual evoked potential study.Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology · 2024
    Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Multivariate Neural Connectivity Patterns in Early Infancy Predict Later Autism Symptoms.Biological psychiatry. Cognitive neuroscience and neuroimaging · 2021
    Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. A MEG Study of Acute Arbaclofen (STX-209) Administration.Frontiers in integrative neuroscience · 2019
    Article
  14. Modeling of Autism Using Organoid Technology.Molecular neurobiology · 2017
    Review
  15. Article
  16. Review
  17. Review
  18. Review
  19. Article
  20. Inhibition-Based Biomarkers for Autism Spectrum Disorder.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2015
    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.

Russell G PortDepartment of Psychiatry, Perelman School of Medicine, University of Pennsylvania Philadelphia, PA, USA.
Michael J GandalSemel Institute for Neuroscience and Human Behavior, University of California at Los Angeles Los Angeles, CA, USA.
Timothy P L RobertsBioengineering Graduate Group, University of Pennsylvania Philadelphia, PA, USA.
Steven J SiegelDepartment of Psychiatry, Perelman School of Medicine, University of Pennsylvania Philadelphia, PA, USA.
Gregory C CarlsonDepartment of Psychiatry, Perelman School of Medicine, University of Pennsylvania Philadelphia, PA, USA.

Funding

NMDA Receptor Hypofunction in the Amygdala of Schizophrenia PatientsP50MH096891 · NIMH · UNIVERSITY OF PENNSYLVANIA · PI BILKER, WARREN B. · 2012 to 2016
$10.6M
NIMH NIH HHS P50 MH096891
6 · The paper itself

Abstract

Most recent estimates indicate that 1 in 68 children are affected by an autism spectrum disorder (ASD). Though decades of research have uncovered much about these disorders, the pathological mechanism remains unknown. Hampering efforts is the seeming inability to integrate findings over the micro to macro scales of study, from changes in molecular, synaptic and cellular function to large-scale brain dysfunction impacting sensory, communicative, motor and cognitive activity. In this review, we describe how studies focusing on neuronal circuit function provide unique context for identifying common neurobiological disease mechanisms of ASD. We discuss how recent EEG and MEG studies in subjects with ASD have repeatedly shown alterations in ensemble population recordings (both in simple evoked related potential latencies and specific frequency subcomponents). Because these disease-associated electrophysiological abnormalities have been recapitulated in rodent models, studying circuit differences in these models may provide access to abnormal circuit function found in ASD. We then identify emerging in vivo and ex vivo techniques, focusing on how these assays can characterize circuit level dysfunction and determine if these abnormalities underlie abnormal clinical electrophysiology. Such circuit level study in animal models may help us understand how diverse genetic and environmental risks can produce a common set of EEG, MEG and anatomical abnormalities found in ASD.

Indexed as

ASDcircuitEEGgammaMEGneurophysiologytranslationalVSDi

Identifiers

PMID25538564
PMCPMC4259121

What OpenQuestion holds

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Registered trials

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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.