Evidence map›Paper›PMID 25018705›Full record

ArticleFrontiers in systems neuroscience2014

Twenty-four hour quantitative-EEG and in-vivo glutamate biosensor detects activity and circadian rhythm dependent biomarkers of pathogenesis in Mecp2 null mice.

Michael V Johnston, Simon Ammanuel, Cliona O'Driscoll, Amy Wozniak, Sakkubai Naidu, Shilpa D Kadam

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

Article in Frontiers in systems neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 14% 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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.

  1. Pooled it
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  7. Article
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  9. Critical periods and Autism Spectrum Disorders, a role for sleep.Neurobiology of sleep and circadian rhythms · 2023
    Article
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  11. Article
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  15. Literature Cases Summarized Based on Their Polysomnographic Findings in Rett Syndrome.International journal of environmental research and public health · 2022
    Review
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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

6 authors at 1 institution in 1 country.

Michael V JohnstonNeuroscience Laboratory, Departments of Neurology and Pediatrics, Hugo Moser Research Institute at Kennedy Krieger, Johns Hopkins University School of Medicine Baltimore, MD, USA.
Simon AmmanuelNeuroscience Laboratory, Hugo Moser Research Institute at Kennedy Krieger Baltimore, MD, USA.
Cliona O'DriscollDepartment of Environmental Health Sciences, Johns Hopkins Bloomberg School of Public Health, Hugo Moser Research Institute at Kennedy Krieger, Johns Hopkins University School of Medicine Baltimore, MD, USA.
Amy WozniakBiostatistics Center, Johns Hopkins Bloomberg School of Public Health, Johns Hopkins University School of Medicine Baltimore, MD, USA.
Sakkubai NaiduDepartments of Neurology and Pediatrics, Hugo Moser Research Institute at Kennedy Krieger Baltimore, MD, USA.
Shilpa D KadamNeuroscience Laboratory, Departments of Neurology, Hugo Moser Research Institute at Kennedy Krieger and Johns Hopkins University School of Medicine Baltimore, MD, USA.
Kennedy Krieger Institute · US

Funding

Neonatal ischemic seizures: age and gender susceptibility to refractorinessR21HD073105 · NICHD · HUGO W. MOSER RES INST KENNEDY KRIEGER · PI KADAM, SHILPA DATTATRAY · 2014 to 2015
$433k
NICHD NIH HHS R21 HD073105
6 · The paper itself

Abstract

Mutations in the X-linked gene encoding methyl-CpG-binding protein 2 (Mecp2) cause most cases of Rett syndrome (RTT). Currently there is no cure for RTT. Abnormal EEGs are found in 100% of RTT cases and are associated with severe sleep dysfunction, the cause of which is not well understood. Mice deficient in MeCP2 protein have been studied and characterized for their neuropathological and behavioral deficits to better understand RTT. With the goal to study the non-ictal EEG correlates in symptomatic Mecp2 KO mice (Mecp2(tm1.1Bird/y)), and determine novel EEG biomarkers of their reported progressive neurodegeneration, we used 24 h video-EEG/EMG with synchronous in-vivo cortical glutamate biosensor in the frontal cortex. We scored the EEG for activity states and spectral analysis was performed to evaluate correlations to the synchronous extracellular glutamate fluctuations underlying Mecp2 inactivation as compared to WT. Significant alterations in sleep structure due to dark cycle-specific long wake states and poor quality of slow-wave sleep were associated with a significant increase in glutamate loads per activity cycle. The dynamics of the activity-state-dependent physiological rise and fall of glutamate indicative of glutamate homeostasis were significantly altered in the KO mice. Colorimetric quantitation of absolute glutamate levels in frontal cortex also indicated the presence of significantly higher levels in KO. This study for the first time found evidence of uncompensated sleep deprivation-like EEG biomarkers that were associated with glutamate homeostatic dysfunction in the Mecp2 KO mice.

Indexed as

biomarkersglutamateMecp2Rett syndromesleep structure

Identifiers

PMID25018705
PMCPMC4072927
OpenAlexW1971930170

What OpenQuestion holds

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LicenceCC BY
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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.