Evidence map›Paper›PMID 33910615›Full record

ArticleMolecular autism2021

Shifted phase of EEG cross-frequency coupling in individuals with Phelan-McDermid syndrome.

Michael G Mariscal, Elizabeth Berry-Kravis, Joseph D Buxbaum, Lauren E Ethridge, Rajna Filip-Dhima, Jennifer H Foss-Feig, Alexander Kolevzon, Meera E Modi, Matthew W Mosconi, Charles A Nelson and 9 more

Open access · goldAbstract read
In one paragraph

Article in Molecular autism, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

11 citing papers in PubMed, 20 citations in OpenAlex.

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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

19 authors at 6 institutions in 1 country.

Michael G MariscalDepartment of Neurology, Boston Children's Hospital, Boston, MA, USA.
Elizabeth Berry-KravisDepartment of Pediatrics, Rush University Medical Center, Chicago, IL, USA.
Joseph D BuxbaumSeaver Autism Center, Icahn School of Medicine at Mount Sinai Hospital, New York, NY, USA.
Lauren E EthridgeDepartment of Pediatrics, University of Oklahoma Health Science Center, Oklahoma City, OK, USA.
Rajna Filip-DhimaDepartment of Neurology, Boston Children's Hospital, Boston, MA, USA.
Jennifer H Foss-FeigSeaver Autism Center, Icahn School of Medicine at Mount Sinai Hospital, New York, NY, USA.
Alexander KolevzonSeaver Autism Center, Icahn School of Medicine at Mount Sinai Hospital, New York, NY, USA.
Meera E ModiDepartment of Neurology, Boston Children's Hospital, Boston, MA, USA.
Matthew W MosconiClinical Child Psychology Program, Schiefelbusch Institute for Life Span Studies, University of Kansas, Lawrence, KS, USA.
Charles A NelsonDepartment of Pediatrics, Boston Children's Hospital, Boston, MA, USA.
Craig M PowellDepartment of Neurobiology, UAB School of Medicine, Birmingham, AL, USA.
Paige M SiperSeaver Autism Center, Icahn School of Medicine at Mount Sinai Hospital, New York, NY, USA.
Latha SooryaDepartment of Psychiatry, Rush University Medical Center, Chicago, IL, USA.
Andrew ThaliathDepartment of Pediatrics, Rush University Medical Center, Chicago, IL, USA.
Audrey ThurmIntramural Research Program, National Institute of Mental Health, Bethesda, USA.
Bo ZhangDepartment of Neurology, Boston Children's Hospital, Boston, MA, USA.
Mustafa SahinDepartment of Neurology, Boston Children's Hospital, Boston, MA, USA.
April R LevinDepartment of Neurology, Boston Children's Hospital, Boston, MA, USA. April.Levin@childrens.harvard.edu.ORCID 0000-0003-4192-4720
Developmental Synaptopathies Consortium
Boston Children's Hospital · USMount Sinai Hospital · USRush University Medical Center · USNational Institute of Mental Health · USUniversity of Kansas · USUniversity of Oklahoma Health Sciences Center · US

Funding

Toward better characterization and clinical trial readiness for targeting neuropsychiatric manifestations in PTEN pathogenic variantsU54NS092090 · NINDS · BOSTON CHILDREN'S HOSPITAL · PI M. Pilar Trelles · 2014 to 2026
$20.1M
Neurodevelopmental and Behavioral Phenotyping ZICMH002961 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI THURM, AUDREY · 2017 to 2025
$12.6M
Mouse Neurodevelopmental Behavior CoreU54HD090255 · NICHD · BOSTON CHILDREN'S HOSPITAL · PI POMEROY, SCOTT LOREN · 2016 to 2020
$5.2M
NOVEL GENETIC MODELS OF AUTISMR01HD069560 · NICHD · UT SOUTHWESTERN MEDICAL CENTER · PI POWELL, CRAIG M · 2011 to 2020
$4.8M
Molecular and Cellular Basis of Neurodevelopmental DisordersR01MH113948 · NIMH · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI POWELL, CRAIG M · 2020 to 2024
$3.3M
Intramural NIH HHS ZIC MH002961NICHD NIH HHS U54 HD090255NIMH NIH HHS R01 MH113948NINDS NIH HHS U54 NS092090
6 · The paper itself

Abstract

backgroundPhelan-McDermid Syndrome (PMS) is a rare condition caused by deletion or mutation of the SHANK3 gene. Individuals with PMS frequently present with intellectual disability, autism spectrum disorder, and other neurodevelopmental challenges. Electroencephalography (EEG) can provide a window into network-level function in PMS.

methodsHere, we analyze EEG data collected across multiple sites in individuals with PMS (n = 26) and typically developing individuals (n = 15). We quantify oscillatory power, alpha-gamma phase-amplitude coupling strength, and phase bias, a measure of the phase of cross frequency coupling thought to reflect the balance of feedforward (bottom-up) and feedback (top-down) activity.

resultsWe find individuals with PMS display increased alpha-gamma phase bias (U = 3.841, p < 0.0005), predominantly over posterior electrodes. Most individuals with PMS demonstrate positive overall phase bias while most typically developing individuals demonstrate negative overall phase bias. Among individuals with PMS, strength of alpha-gamma phase-amplitude coupling was associated with Sameness, Ritualistic, and Compulsive behaviors as measured by the Repetitive Behavior Scales-Revised (Beta = 0.545, p = 0.011).

conclusionsIncreased phase bias suggests potential circuit-level mechanisms underlying phenotype in PMS, offering opportunities for back-translation of findings into animal models and targeting in clinical trials.

Indexed as

Autism Spectrum DisorderChromosome DeletionChromosome DisordersChromosomes, Human, Pair 22ElectroencephalographyHumansCross-frequency couplingEEGPhase biasPhelan-McDermid syndromePower

Identifiers

PMID33910615
PMCPMC8082621
OpenAlexW3142482967

What OpenQuestion holds

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LicenceCC BY
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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.