Evidence map›Paper›PMID 24507514›Full record

ReviewHandbook of clinical neurology2014

Demyelination in multiple sclerosis.

Catherine Lubetzki, Bruno Stankoff

Abstract readReview
In one paragraph

Review in Handbook of clinical neurology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed, 5 pooled it
29.7field-weighted citation impact, top 1% 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

86 citing papers in PubMed, 5 syntheses or guidelines pooled it, 139 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Ofatumumab therapy modulates the meningeal lymphatic draining function in patients with multiple sclerosis: a pilot study.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. A computational roadmap to activity-dependent myelination.Frontiers in computational neuroscience · 2026
    Article
  19. Ophthalmic conditions in patients with multiple sclerosis.Multiple sclerosis and related disorders · 2025
    Article
  20. Article

26 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

2 authors at 1 institution in 1 country.

Catherine LubetzkiCentre de Recherche de l'Institut du Cerveau et de la Moelle Épinière, Salpêtrière Hospital, UMR S975, Paris, France. Electronic address: catherine.lubetzki@psl.aphp.fr.
Bruno StankoffCentre de Recherche de l'Institut du Cerveau et de la Moelle Épinière, Salpêtrière Hospital, UMR S975, Paris, France.
Institut du Cerveau · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This review, focused on demyelination in multiple sclerosis, is divided in two parts. The first part addresses the many and not exclusive mechanisms leading to demyelination in the central nervous system. Although the hypothesis that a primary oligodendrocyte or myelin injury induces a secondary immune response in the central nervous system is still a matter of debate, most recent advances underline the influence of a primary immune response against myelin antigen(s), with a diversity of potential targets. Whereas multiple sclerosis was long considered as a T cell-mediated disease, the role of B lymphocytes is now increasingly recognized, and the influence of antibodies on tissue damage actively investigated. The second part of the review describes the axonal consequences of demyelination. Segmental demyelination results in conduction block or slowing of conduction through adaptative responses, notably related to modifications in the distribution of voltage gated sodium channels along the denuded axon. If demyelination persists, these changes, as well as the loss of trophic and metabolic support, will lead to irreversible axonal damage and loss. In this respect, favouring early myelin repair, during a window of time when axonal damage is still reversible, might pave the way for neuroprotection.

Indexed as

AnimalsAxonsDemyelinating DiseasesHumansMultiple SclerosisMyelin SheathOligodendrogliaSodium ChannelsSodium Channelsadaptive immunityantibodiesantigensautoimmunitycytokinesinflammationinjuryinnate immunitymechanismsmyelin proteinsneuronal damageoligodendrocytes

Identifiers

PMID24507514
PMCPMC7152443
OpenAlexW94241605

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.