Evidence map›Paper›PMID 33196637›Full record

ArticlePLoS biology2020

Structural myelin defects are associated with low axonal ATP levels but rapid recovery from energy deprivation in a mouse model of spastic paraplegia.

Andrea Trevisiol, Kathrin Kusch, Anna M Steyer, Ingo Gregor, Christos Nardis, Ulrike Winkler, Susanne Köhler, Alejandro Restrepo, Wiebke Möbius, Hauke B Werner and 2 more

Abstract read
In one paragraph

Article in PLoS biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

  1. Article
  2. Review
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  5. Oligodendrocytes: Myelination, Plasticity, and Axonal Support.Cold Spring Harbor perspectives in biology · 2024
    Review
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  7. Article
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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.

Andrea TrevisiolDepartment of Neurogenetics, Max Planck Institute of Experimental Medicine, Göttingen, Germany.
Kathrin KuschDepartment of Neurogenetics, Max Planck Institute of Experimental Medicine, Göttingen, Germany.ORCID 0000-0002-5079-502X
Anna M SteyerDepartment of Neurogenetics, Max Planck Institute of Experimental Medicine, Göttingen, Germany.ORCID 0000-0002-4814-7517
Ingo GregorThird Institute of Physics, Georg August University, Göttingen, Germany.ORCID 0000-0002-1775-2159
Christos NardisDepartment of Neurogenetics, Max Planck Institute of Experimental Medicine, Göttingen, Germany.
Ulrike WinklerCarl Ludwig Institute for Physiology, Faculty of Medicine, University of Leipzig, Leipzig, Germany.
Susanne KöhlerCarl Ludwig Institute for Physiology, Faculty of Medicine, University of Leipzig, Leipzig, Germany.
Alejandro RestrepoDepartment of Neurogenetics, Max Planck Institute of Experimental Medicine, Göttingen, Germany.
Wiebke MöbiusDepartment of Neurogenetics, Max Planck Institute of Experimental Medicine, Göttingen, Germany.ORCID 0000-0002-2902-7165
Hauke B WernerDepartment of Neurogenetics, Max Planck Institute of Experimental Medicine, Göttingen, Germany.ORCID 0000-0002-7710-5738
Klaus-Armin NaveDepartment of Neurogenetics, Max Planck Institute of Experimental Medicine, Göttingen, Germany.
Johannes HirrlingerDepartment of Neurogenetics, Max Planck Institute of Experimental Medicine, Göttingen, Germany.ORCID 0000-0002-6327-0089

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In several neurodegenerative disorders, axonal pathology may originate from impaired oligodendrocyte-to-axon support of energy substrates. We previously established transgenic mice that allow measuring axonal ATP levels in electrically active optic nerves. Here, we utilize this technique to explore axonal ATP dynamics in the Plpnull/y mouse model of spastic paraplegia. Optic nerves from Plpnull/y mice exhibited lower and more variable basal axonal ATP levels and reduced compound action potential (CAP) amplitudes, providing a missing link between axonal pathology and a role of oligodendrocytes in brain energy metabolism. Surprisingly, when Plpnull/y optic nerves are challenged with transient glucose deprivation, both ATP levels and CAP decline slower, but recover faster upon reperfusion of glucose. Structurally, myelin sheaths display an increased frequency of cytosolic channels comprising glucose and monocarboxylate transporters, possibly facilitating accessibility of energy substrates to the axon. These data imply that complex metabolic alterations of the axon-myelin unit contribute to the phenotype of Plpnull/y mice.

Indexed as

Action PotentialsAdenosine TriphosphateAnimalsAxonsDisease Models, AnimalEnergy MetabolismFemaleMaleMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicMicroscopy, Electron, TransmissionMicroscopy, ImmunoelectronMyelin Proteolipid ProteinMyelin SheathAdenosine TriphosphateMyelin Proteolipid ProteinPlp1 protein, mouse

Identifiers

PMID33196637
PMCPMC7704050

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.