Evidence map›Paper›PMID 21988534›Full record

ArticleBrain pathology (Zurich, Switzerland)2012

Axonopathy is associated with complex axonal transport defects in a model of multiple sclerosis.

Mihaela Kreutzer, Frauke Seehusen, Robert Kreutzer, Kidsadagorn Pringproa, Maren Kummerfeld, Peter Claus, Ulrich Deschl, Arno Kalkul, Andreas Beineke, Wolfgang Baumgärtner and 1 more

Open access · greenAbstract read
In one paragraph

Article in Brain pathology (Zurich, Switzerland), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

28 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
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  4. Ovalbumin-specific CD4Frontiers in immunology · 2023
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  10. Neurotrophic effects of GScientific reports · 2020
    Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Cytotoxic CD8Brain pathology (Zurich, Switzerland) · 2018
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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

11 authors at 2 institutions in 1 country.

Mihaela KreutzerDepartment of Pathology, University of Veterinary Medicine, Hannover, Germany.
Frauke Seehusen
Robert Kreutzer
Kidsadagorn Pringproa
Maren Kummerfeld
Peter Claus
Ulrich Deschl
Arno Kalkul
Andreas Beineke
Wolfgang Baumgärtner
Reiner Ulrich
University of Veterinary Medicine Hannover, Foundation · DEMedizinische Hochschule Hannover · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple sclerosis (MS) is an inflammatory and neurodegenerative disease characterized by myelin and axonal pathology. In a viral model of MS, we tested whether axonopathy initiation and development are based on an impaired transport of neurofilaments. Spinal cords of Theiler's murine encephalomyelitis virus (TMEV)-infected and mock-infected mice and TMEV infected neuroblastoma N1E-115 cells were analyzed by microarray analysis, light microscopy and electron and laser confocal microscopy. In vivo axonal accumulation of non-phosphorylated neurofilaments after TMEV infection revealed a temporal development caused by the impairments of the axonal traffic consisting of the downregulation of kinesin family member 5A, dynein cytoplasmic heavy chain 1, tau-1 and β-tubulin III expression. In addition, alterations of the protein metabolism were also noticed. In vitro, the TMEV-infected N1E-115 cells developed tandem-repeated swellings similar to in vivo alterations. Furthermore, the hypothesis of an underlying axonal self-destruction program involving nicotinamide adenine dinucleotide depletion was supported by molecular findings. The obtained data indicate that neurofilament accumulation in TME is mainly the result of dysregulation of their axonal transport machinery and impairment of neurofilament phosphorylation and protein metabolism. The present findings allow a more precise understanding of the complex interactions responsible for initiation and development of axonopathies in inflammatory degenerative diseases.

Indexed as

TheilovirusAnimalsAxonal TransportCardiovirus InfectionsDisease Models, AnimalFemaleFluorescent Antibody TechniqueImmunohistochemistryMiceMicroarray AnalysisMicroscopy, ConfocalMicroscopy, Electron, TransmissionMultiple SclerosisNerve DegenerationNeurofilament ProteinsSpinal CordNeurofilament Proteins

Identifiers

PMID21988534
PMCPMC8092950
OpenAlexW2155274741

What OpenQuestion holds

Textmetadata
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.