Evidence map›Paper›PMID 25623793›Full record

ReviewNature reviews. Neurology2015

Autoimmune antigenic targets at the node of Ranvier in demyelinating disorders.

Panos Stathopoulos, Harry Alexopoulos, Marinos C Dalakas

Registry-linked trialAbstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Neurology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04664647 (The Clinical Features of Combined Central and Peripheral Demyelination), which is not on this map. Cited by 66 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 3 pooled it
8.4field-weighted citation impact, top 2% 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.

NCT04664647 unknown statusnot on this mapstarted 2020, after this paper: background citation

The Clinical Features of Combined Central and Peripheral Demyelination

TypeobservationalSponsorXuanwu Hospital, BeijingRan2020 to 2021Enrolled30ConditionsCombined Central and Peripheral Demyelination Disease
3 · Its place in the literature

Who cites it

66 citing papers in PubMed, 3 syntheses or guidelines pooled it, 116 citations in OpenAlex.

  1. Pooled it
  2. Guillain Barre Syndrome as a Complication of COVID-19: A Systematic Review.The Canadian journal of neurological sciences. Le journal canadien des sciences neurologiques · 2022
    Pooled it
  3. Pooled it
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Antibody-Mediated Nodo- and Paranodopathies.Journal of clinical medicine · 2024
    Review
  14. Review
  15. Review
  16. Review
  17. Growing Spectrum of Autoimmune Nodopathies.Current neurology and neuroscience reports · 2023
    Review
  18. Article
  19. Review
  20. Article

6 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

3 authors at 1 institution in 1 country.

Panos StathopoulosNeuroimmunology Unit, Department of Pathophysiology, Faculty of Medicine, National and Kapodistrian University of Athens, 75 Mikras Asias Street, Goudi, Athens 11527, Greece.
Harry AlexopoulosNeuroimmunology Unit, Department of Pathophysiology, Faculty of Medicine, National and Kapodistrian University of Athens, 75 Mikras Asias Street, Goudi, Athens 11527, Greece.
Marinos C DalakasNeuroimmunology Unit, Department of Pathophysiology, Faculty of Medicine, National and Kapodistrian University of Athens, 75 Mikras Asias Street, Goudi, Athens 11527, Greece.
National and Kapodistrian University of Athens · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mounting evidence suggests that autoantibodies contribute to the pathogenesis of demyelination in the PNS and CNS. Rapid reversal of electrophysiological blockade after plasmapheresis or intravenous immunoglobulin treatment for acute or chronic inflammatory demyelinating polyneuropathy is more likely to result from removal or neutralization of an antibody that impairs saltatory conduction than from remyelination. Although up to 30% of patients with acute or chronic inflammatory demyelinating polyneuropathy harbour autoantibodies, specific antigens have been identified in no more than 13% of cases. To date, autoantigens identified at the node of Ranvier include neurofascin 186, gliomedin and possibly moesin in the nodal domain, and contactin-1, Caspr1 and neurofascin 155 in the paranodal domain. In some patients with multiple sclerosis, paranodal CNPase and juxtaparanodal contactin-2 trigger a humoral response. This Review explores the molecular anatomy of the node of Ranvier, focusing on proteins with extracellular domains that could serve as antigens. The clinical implications of node-specific antibody responses are addressed, and the best approaches to identify antibodies that target nodal proteins are highlighted. Also discussed are the roles of these antibodies as either secondary, disease-exacerbating responses, or as a primary effector mechanism that defines demyelination or axonal degeneration at the node, identifies disease subtypes or determines response to treatments.

Indexed as

AnimalsAutoantibodiesAutoantigensDemyelinating DiseasesHumansRanvier's NodesAutoantibodiesAutoantigens

Identifiers

PMID25623793
OpenAlexW1967064220

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.