Evidence map›Paper›PMID 20840067›Full record

ReviewCurrent drug targets2010

Skeletal muscle in motor neuron diseases: therapeutic target and delivery route for potential treatments.

Luc Dupuis, Andoni Echaniz-Laguna

Abstract readReview
In one paragraph

Review in Current drug targets, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.5field-weighted citation impact, top 12% 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

27 citing papers in PubMed, 50 citations in OpenAlex.

  1. Delayed-Onset Muscle Soreness Begins with a Transient Neural Switch.International journal of molecular sciences · 2025
    Review
  2. Sorting differentiated mammalian cells using deterministic lateral displacement microfluidic devices.Analytical sciences : the international journal of the Japan Society for Analytical Chemistry · 2024
    Article
  3. Genes · 2024
    Review
  4. Review
  5. Article
  6. Article
  7. The Cellular and Molecular Signature of ALS in Muscle.Journal of personalized medicine · 2022
    Review
  8. Article
  9. Article
  10. Article
  11. Neurodegeneration and axonal mRNA transportation.American journal of neurodegenerative disease · 2021
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Synaptic Failure: Focus in an Integrative View of ALS.Brain plasticity (Amsterdam, Netherlands) · 2016
    Review
  17. Deficiency of the Survival of Motor Neuron Protein Impairs mRNA Localization and Local Translation in the Growth Cone of Motor Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  18. Article
  19. Article
  20. Article
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.

Luc DupuisInserm, U692, Strasbourg, F-67085 France. ldupuis@unistra.fr
Andoni Echaniz-Laguna
Inserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lower motor neuron (LMN) degeneration occurs in several diseases that affect patients from neonates to elderly and can either be genetically transmitted or occur sporadically. Among diseases involving LMN degeneration, spinal muscular atrophy (SMA) and spinal bulbar muscular atrophy (Kennedy's disease, SBMA) are pure genetic diseases linked to loss of the SMN gene (SMA) or expansion of a polyglutamine tract in the androgen receptor gene (SBMA) while amyotrophic lateral sclerosis (ALS) can either be of genetic origin or occur sporadically. In this review, our aim is to put forward the hypothesis that muscle fiber atrophy and weakness might not be a simple collateral damage of LMN degeneration, but instead that muscle fibers may be the site of crucial pathogenic events in these diseases. In SMA, the SMN gene was shown to be required for muscle structure and strength as well as for neuromuscular junction formation, and a subset of SMA patients develop myopathic pathology. In SBMA, the occurrence of myopathic histopathology in patients and animal models, along with neuromuscular phenotype of animal models expressing the androgen receptor in muscle only has lead to the proposal that SBMA may indeed be a muscle disease. Lastly, in ALS, at least part of the phenotype might be explained by pathogenic events occuring in skeletal muscle. Apart from its potential pathogenic role, skeletal muscle pathophysiological events might be a target for treatments and/or be a preferential route for targeting motor neurons.

Indexed as

Drug Delivery SystemsAnimalsHumansMotor Neuron DiseaseMotor NeuronsMuscle Fibers, SkeletalMuscle, SkeletalMuscular Atrophy

Identifiers

PMID20840067
PMCPMC4834127
OpenAlexW2004405584

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.