Evidence map›Paper›PMID 27633977›Full record

ReviewThe Journal of physiology2017

New perspectives on amyotrophic lateral sclerosis: the role of glial cells at the neuromuscular junction.

Danielle Arbour, Christine Vande Velde, Richard Robitaille

Open access · greenAbstract readReview
In one paragraph

Review in The Journal of physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

55 citing papers in PubMed, 73 citations in OpenAlex.

  1. Trial
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  4. Muscle-Derived BMP4 Regulates Morphology and Function of Endplates on Extrafusal and Intrafusal Muscle Fibers in Adult Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026
    Article
  5. The Neuromuscular Junction: A Shared Vulnerability in Aging and Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Review
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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

3 authors at 2 institutions in 1 country.

Danielle ArbourDépartement de neurosciences, Université de Montréal, Montréal, Québec, Canada, H3C 3J7.
Christine Vande VeldeDépartement de neurosciences, Université de Montréal, Montréal, Québec, Canada, H3C 3J7.
Richard RobitailleDépartement de neurosciences, Université de Montréal, Montréal, Québec, Canada, H3C 3J7.
Université de Montréal · CACentre Hospitalier de l’Université de Montréal · CA

Funding

CIHR
6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) is a disease leading to the death of motor neurons (MNs). It is also recognized as a non-cell autonomous disease where glial cells in the CNS are involved in its pathogenesis and progression. However, although denervation of neuromuscular junctions (NMJs) represents an early and major event in ALS, the importance of glial cells at this synapse receives little attention. An interesting possibility is that altered relationships between glial cells and MNs in the spinal cord in ALS may also take place at the NMJ. Perisynaptic Schwann cells (PSCs), which are glial cells at the NMJ, show great morphological and functional adaptability to ensure NMJ stability, maintenance and repair. More specifically, PSCs change their properties according to the state of innervation. Hence, abnormal changes or lack of changes can have detrimental effects on NMJs in ALS. This review will provide an overview of known and hypothesized interactions between MN nerve terminals and PSCs at NMJs during development, aging and ALS-induced denervation. These neuron-PSC interactions may be crucial to the understanding of how degenerative changes begin and progress at NMJs in ALS, and represent a novel therapeutic target.

Indexed as

Amyotrophic Lateral SclerosisAnimalsHumansMotor NeuronsNeurogliaNeuromuscular Junctiondenervationmotor unitnon-cell autonomyperisynaptic Schwann cellsre-innervationremodelingSOD1synaptic transmission

Identifiers

PMID27633977
PMCPMC5285712
OpenAlexW2559777674

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.