Evidence map›Paper›PMID 19158292›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009

Non-nuclear Wld(S) determines its neuroprotective efficacy for axons and synapses in vivo.

Bogdan Beirowski, Elisabetta Babetto, Jon Gilley, Francesca Mazzola, Laura Conforti, Lucie Janeckova, Giulio Magni, Richard R Ribchester, Michael P Coleman

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
5.8field-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

62 citing papers in PubMed, 98 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. SARM1-Dependent Axon Degeneration: Nucleotide Signaling, Neurodegenerative Disorders, Toxicity, and Therapeutic Opportunities.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2024
    Review
  6. Review
  7. Role of NADCellular and molecular neurobiology · 2023
    Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. Identification of evolutionary and kinetic drivers of NAD-dependent signaling.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  16. Sarm1 Deletion, but Not WldCell reports · 2017
    Article
  17. Axon degeneration: make the Schwann cell great again.Neural regeneration research · 2017
    Review
  18. Nicotinamide and WLDFrontiers in neuroscience · 2017
    Article
  19. Rescue of Glaucomatous Neurodegeneration by Differentially Modulating Neuronal Endoplasmic Reticulum Stress Molecules.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  20. Retrograde Axonal Degeneration in Parkinson Disease.Journal of Parkinson's disease · 2016
    Review

2 more citing papers are in PubMed but not listed here.

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

9 authors at 2 institutions in 1 country.

Bogdan BeirowskiLaboratory of Molecular Signalling, The Babraham Institute, Cambridge, UK.
Elisabetta Babetto
Jon Gilley
Francesca Mazzola
Laura Conforti
Lucie Janeckova
Giulio Magni
Richard R Ribchester
Michael P Coleman
Babraham Institute · GBUniversity of Edinburgh · GB

Funding

Biotechnology and Biological Sciences Research CouncilMedical Research Council G0300408Medical Research Council G0401091
6 · The paper itself

Abstract

Axon degeneration contributes widely to neurodegenerative disease but its regulation is poorly understood. The Wallerian degeneration slow (Wld(S)) protein protects axons dose-dependently in many circumstances but is paradoxically abundant in nuclei. To test the hypothesis that Wld(S) acts within nuclei in vivo, we redistributed it from nucleus to cytoplasm in transgenic mice. Surprisingly, instead of weakening the phenotype as expected, extranuclear Wld(S) significantly enhanced structural and functional preservation of transected distal axons and their synapses. In contrast to native Wld(S) mutants, distal axon stumps remained continuous and ultrastructurally intact up to 7 weeks after injury and motor nerve terminals were robustly preserved even in older mice, remaining functional for 6 d. Moreover, we detect extranuclear Wld(S) for the first time in vivo, and higher axoplasmic levels in transgenic mice with Wld(S) redistribution. Cytoplasmic Wld(S) fractionated predominantly with mitochondria and microsomes. We conclude that Wld(S) can act in one or more non-nuclear compartments to protect axons and synapses, and that molecular changes can enhance its therapeutic potential.

Indexed as

Age FactorsAlanineAmyloid beta-Protein PrecursorAnalysis of VarianceAnimalsArginineAxonsCell Line, TransformedDenervationDisease Models, AnimalElectromyographyHumansLuminescent ProteinsMiceMice, TransgenicMicroscopy, Electron, TransmissionAlanineAmyloid beta-Protein PrecursorArginineLuminescent ProteinsMitochondrial ProteinsNerve Tissue ProteinsTubb3 protein, ratTubulinWld protein, mouse

Identifiers

PMID19158292
PMCPMC6665162
OpenAlexW2059034896

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.