Evidence map›Paper›PMID 27470661›Full record

ArticleGlia2016

Cortical network dysfunction caused by a subtle defect of myelination.

Giulia Poggi, Susann Boretius, Wiebke Möbius, Nicole Moschny, Jürgen Baudewig, Torben Ruhwedel, Imam Hassouna, Georg L Wieser, Hauke B Werner, Sandra Goebbels and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Glia, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
8.8field-weighted citation impact, top 2% 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

40 citing papers in PubMed, 74 citations in OpenAlex.

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  8. Myelin in Alzheimer's disease: culprit or bystander?Acta neuropathologica communications · 2023
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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

12 authors at 3 institutions in 2 countries.

Giulia PoggiClinical Neuroscience, Max Planck Institute of Experimental Medicine, Göttingen.
Susann BoretiusDepartment of Radiology and Neuroradiology, Christian-Albrechts-University, Kiel.
Wiebke MöbiusNeurogenetics, Max Planck Institute of Experimental Medicine, Göttingen.
Nicole MoschnyClinical Neuroscience, Max Planck Institute of Experimental Medicine, Göttingen.
Jürgen BaudewigDepartment of Radiology and Neuroradiology, Christian-Albrechts-University, Kiel.
Torben RuhwedelNeurogenetics, Max Planck Institute of Experimental Medicine, Göttingen.
Imam HassounaClinical Neuroscience, Max Planck Institute of Experimental Medicine, Göttingen.
Georg L WieserNeurogenetics, Max Planck Institute of Experimental Medicine, Göttingen.
Hauke B WernerNeurogenetics, Max Planck Institute of Experimental Medicine, Göttingen.
Sandra GoebbelsNeurogenetics, Max Planck Institute of Experimental Medicine, Göttingen.
Klaus-Armin NaveNeurogenetics, Max Planck Institute of Experimental Medicine, Göttingen. nave@em.mpg.de.
Hannelore EhrenreichClinical Neuroscience, Max Planck Institute of Experimental Medicine, Göttingen. ehrenreich@em.mpg.de.
Max Planck Institute of Experimental Medicine · DEKiel University · DENanoscale Microscopy and Molecular Physiology of the Brain Cluster of Excellence 171 — DFG Research Center 103 · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Subtle white matter abnormalities have emerged as a hallmark of brain alterations in magnetic resonance imaging or upon autopsy of mentally ill subjects. However, it is unknown whether such reduction of white matter and myelin contributes to any disease-relevant phenotype or simply constitutes an epiphenomenon, possibly even treatment-related. Here, we have re-analyzed Mbp heterozygous mice, the unaffected parental strain of shiverer, a classical neurological mutant. Between 2 and 20 months of age, Mbp(+/-) versus Mbp(+/+) littermates were deeply phenotyped by combining extensive behavioral/cognitive testing with MRI, 1H-MR spectroscopy, electron microscopy, and molecular techniques. Surprisingly, Mbp-dependent myelination was significantly reduced in the prefrontal cortex. We also noticed a mild but progressive hypomyelination of the prefrontal corpus callosum and low-grade inflammation. While most behavioral functions were preserved, Mbp(+/-) mice exhibited defects of sensorimotor gating, as evidenced by reduced prepulse-inhibition, and a late-onset catatonia phenotype. Thus, subtle but primary abnormalities of CNS myelin can be the cause of a persistent cortical network dysfunction including catatonia, features typical of neuropsychiatric conditions. GLIA 2016;64:2025-2040.

Indexed as

2',3'-Cyclic Nucleotide 3'-PhosphodiesteraseAge FactorsAnimalsDisease Models, AnimalExploratory BehaviorFemaleLeukoencephalopathiesMaze LearningMiceMice, Inbred C57BLMice, TransgenicMicrogliaMyelin Basic ProteinMyelin SheathNeural PathwaysNitric Oxide Synthase Type II2',3'-Cyclic Nucleotide 3'-PhosphodiesteraseCnp protein, mouseMyelin Basic ProteinNitric Oxide Synthase Type IIcatatoniaCnp mutantelectron microscopyMRImyelin basic protein (Mbp) mutantprepulse inhibition

Identifiers

PMID27470661
PMCPMC5129527
OpenAlexW2486213928

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

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.