Evidence map›Paper›PMID 28082868›Full record

ReviewFrontiers in molecular neuroscience2016

Neuromuscular Junction Impairment in Amyotrophic Lateral Sclerosis: Reassessing the Role of Acetylcholinesterase.

Maria-Letizia Campanari, María-Salud García-Ayllón, Sorana Ciura, Javier Sáez-Valero, Edor Kabashi

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in molecular neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
6.1field-weighted citation impact, top 4% 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

37 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
  2. Validation in Drosophila of the in silico predicted clomipramine as repurposable for SOD1-ALS.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
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  3. Article
  4. Review
  5. Real-time monitoring andJournal of pharmaceutical analysis · 2025
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  8. Article
  9. Review
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  11. Review
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  15. Boosting the peripheral immune response in the skeletal muscles improved motor function in ALS transgenic mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2022
    Article
  16. Article
  17. Article
  18. Article
  19. Review
  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

5 authors at 2 institutions in 2 countries.

Maria-Letizia CampanariSorbonne Université, Université Pierre et Marie Curie (UPMC), Université de Paris 06, Unité Mixte 75, Institut National de la Santé et de la Recherche Médicale (INSERM) Unité 1127, Centre National de la Recherche Scientifique (CNRS) Unité Mixte de Recherche 7225 Institut du Cerveau et de la Moelle Épinière (ICM) Paris, France.
María-Salud García-AyllónInstituto de Neurociencias de Alicante, Universidad Miguel Hernández-CSIC, Sant Joan d'AlacantSpain; Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED)Madrid, Spain; Unidad de Investigación, Hospital General Universitario de Elche, FISABIOElche, Spain.
Sorana CiuraSorbonne Université, Université Pierre et Marie Curie (UPMC), Université de Paris 06, Unité Mixte 75, Institut National de la Santé et de la Recherche Médicale (INSERM) Unité 1127, Centre National de la Recherche Scientifique (CNRS) Unité Mixte de Recherche 7225 Institut du Cerveau et de la Moelle Épinière (ICM) Paris, France.
Javier Sáez-ValeroInstituto de Neurociencias de Alicante, Universidad Miguel Hernández-CSIC, Sant Joan d'AlacantSpain; Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED)Madrid, Spain.
Edor KabashiSorbonne Université, Université Pierre et Marie Curie (UPMC), Université de Paris 06, Unité Mixte 75, Institut National de la Santé et de la Recherche Médicale (INSERM) Unité 1127, Centre National de la Recherche Scientifique (CNRS) Unité Mixte de Recherche 7225 Institut du Cerveau et de la Moelle Épinière (ICM) Paris, France.
Institut du Cerveau · FRBiomedical Research Networking Center on Neurodegenerative Diseases · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amyotrophic Lateral Sclerosis (ALS) is a highly debilitating disease caused by progressive degeneration of motorneurons (MNs). Due to the wide variety of genes and mutations identified in ALS, a highly varied etiology could ultimately converge to produce similar clinical symptoms. A major hypothesis in ALS research is the "distal axonopathy" with pathological changes occurring at the neuromuscular junction (NMJ), at very early stages of the disease, prior to MNs degeneration and onset of clinical symptoms. The NMJ is a highly specialized cholinergic synapse, allowing signaling between muscle and nerve necessary for skeletal muscle function. This nerve-muscle contact is characterized by the clustering of the collagen-tailed form of acetylcholinesterase (ColQ-AChE), together with other components of the extracellular matrix (ECM) and specific key molecules in the NMJ formation. Interestingly, in addition to their cholinergic role AChE is thought to play several "non-classical" roles that do not require catalytic function, most prominent among these is the facilitation of neurite growth, NMJ formation and survival. In all this context, abnormalities of AChE content have been found in plasma of ALS patients, in which AChE changes may reflect the neuromuscular disruption. We review these findings and particularly the evidences of changes of AChE at neuromuscular synapse in the pre-symptomatic stages of ALS.

Indexed as

acetylcholinesterase (AChE)amyotrophic lateral sclerosis (ALS)axonopathycollagen tail subunit of asymmetric acetylcholinesterase (ColQ)neuromuscular junction (NMJ)

Identifiers

PMID28082868
PMCPMC5187284
OpenAlexW2562417922

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.