Evidence map›Paper›PMID 30072689›Full record

ArticleNature communications2018

Targeting myelin lipid metabolism as a potential therapeutic strategy in a model of CMT1A neuropathy.

R Fledrich, T Abdelaal, L Rasch, V Bansal, V Schütza, B Brügger, C Lüchtenborg, T Prukop, J Stenzel, R U Rahman and 15 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed, 1 pooled it
5.7field-weighted citation impact, top 3% 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

59 citing papers in PubMed, 1 synthesis or guideline pooled it, 118 citations in OpenAlex.

  1. Pooled it
  2. Review
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  5. Article
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  7. Article
  8. Review
  9. Basic Pathological Mechanisms in Peripheral Nerve Diseases.International journal of molecular sciences · 2025
    Review
  10. Article
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  12. Dynamic regulation ofFrontiers in cell and developmental biology · 2025
    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

25 authors at 9 institutions in 2 countries.

R FledrichDepartment of Neurogenetics, Max-Planck-Institute of Experimental Medicine, Göttingen, 37075, Germany. fledrich@em.mpg.de.ORCID http://orcid.org/0000-0001-5323-7958
T AbdelaalDepartment of Neurogenetics, Max-Planck-Institute of Experimental Medicine, Göttingen, 37075, Germany.ORCID http://orcid.org/0000-0003-4693-7379
L RaschDepartment of Neurogenetics, Max-Planck-Institute of Experimental Medicine, Göttingen, 37075, Germany.
V BansalCenter for Molecular Neurobiology, Institute of Medical Systems Biology, University Medical Center Hamburg-Eppendorf, Hamburg, 20251, Germany.
V SchützaDepartment of Neurogenetics, Max-Planck-Institute of Experimental Medicine, Göttingen, 37075, Germany.
B BrüggerHeidelberg University Biochemistry Center (BZH), Heidelberg, 69120, Germany.
C LüchtenborgHeidelberg University Biochemistry Center (BZH), Heidelberg, 69120, Germany.
T PrukopDepartment of Neurogenetics, Max-Planck-Institute of Experimental Medicine, Göttingen, 37075, Germany.
J StenzelDepartment of Neurogenetics, Max-Planck-Institute of Experimental Medicine, Göttingen, 37075, Germany.
R U RahmanCenter for Molecular Neurobiology, Institute of Medical Systems Biology, University Medical Center Hamburg-Eppendorf, Hamburg, 20251, Germany.
D HermesDepartment of Neurogenetics, Max-Planck-Institute of Experimental Medicine, Göttingen, 37075, Germany.ORCID http://orcid.org/0000-0002-1779-093X
D EwersDepartment of Neurogenetics, Max-Planck-Institute of Experimental Medicine, Göttingen, 37075, Germany.ORCID http://orcid.org/0000-0003-1037-1027
W MöbiusDepartment of Neurogenetics, Max-Planck-Institute of Experimental Medicine, Göttingen, 37075, Germany.ORCID http://orcid.org/0000-0002-2902-7165
T RuhwedelDepartment of Neurogenetics, Max-Planck-Institute of Experimental Medicine, Göttingen, 37075, Germany.
I KatonaInstitute of Neuropathology, University Hospital Aachen, Aachen, 52074, Germany.ORCID http://orcid.org/0000-0002-0955-8911
J WeisInstitute of Neuropathology, University Hospital Aachen, Aachen, 52074, Germany.
D KleinDepartment of Neurology, Section of Developmental Neurobiology, University Hospital Wuerzburg, Wuerzburg, 97080, Germany.
R MartiniDepartment of Neurology, Section of Developmental Neurobiology, University Hospital Wuerzburg, Wuerzburg, 97080, Germany.
W BrückInstitute of Neuropathology, University Medical Center Göttingen, Göttingen, 37075, Germany.
W C MüllerDepartment of Neuropathology, University Hospital Leipzig, Leipzig, 04103, Germany.
S BonnCenter for Molecular Neurobiology, Institute of Medical Systems Biology, University Medical Center Hamburg-Eppendorf, Hamburg, 20251, Germany.ORCID http://orcid.org/0000-0003-4366-5662
I BechmannInstitute of Anatomy, University of Leipzig, Leipzig, 04103, Germany.
K A NaveDepartment of Neurogenetics, Max-Planck-Institute of Experimental Medicine, Göttingen, 37075, Germany. nave@em.mpg.de.
R M StassartDepartment of Neurogenetics, Max-Planck-Institute of Experimental Medicine, Göttingen, 37075, Germany. stassart@em.mpg.de.ORCID http://orcid.org/0000-0002-5919-1652
M W SeredaDepartment of Neurogenetics, Max-Planck-Institute of Experimental Medicine, Göttingen, 37075, Germany. sereda@em.mpg.de.
Universitätsmedizin Göttingen · DEUniversität Hamburg · DEUniversity Hospital Leipzig · DEHeidelberg University · DEMax Planck Institute of Experimental Medicine · DEUniversitätsklinikum Aachen · DEUniversitätsklinikum Würzburg · DELeipzig University · DENanoscale Microscopy and Molecular Physiology of the Brain Cluster of Excellence 171 — DFG Research Center 103 · DE

Funding

Bundesministerium für Bildung und Forschung (Federal Ministry of Education and Research) 01GM1511C
6 · The paper itself

Abstract

In patients with Charcot-Marie-Tooth disease 1A (CMT1A), peripheral nerves display aberrant myelination during postnatal development, followed by slowly progressive demyelination and axonal loss during adult life. Here, we show that myelinating Schwann cells in a rat model of CMT1A exhibit a developmental defect that includes reduced transcription of genes required for myelin lipid biosynthesis. Consequently, lipid incorporation into myelin is reduced, leading to an overall distorted stoichiometry of myelin proteins and lipids with ultrastructural changes of the myelin sheath. Substitution of phosphatidylcholine and phosphatidylethanolamine in the diet is sufficient to overcome the myelination deficit of affected Schwann cells in vivo. This treatment rescues the number of myelinated axons in the peripheral nerves of the CMT rats and leads to a marked amelioration of neuropathic symptoms. We propose that lipid supplementation is an easily translatable potential therapeutic approach in CMT1A and possibly other dysmyelinating neuropathies.

Indexed as

Lipid MetabolismAnimalsAxonsCharcot-Marie-Tooth DiseaseDietary FatsLipidsMyelin SheathPhospholipidsRats, TransgenicSchwann CellsDietary FatsLipidsPhospholipids

Identifiers

PMID30072689
PMCPMC6072747
OpenAlexW2883223685

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.