Evidence map›Paper›PMID 34997540›Full record

ReviewMolecular neurobiology2022

Neuromuscular Junction Dysfunction in Amyotrophic Lateral Sclerosis.

Sagar Verma, Shiffali Khurana, Abhishek Vats, Bandana Sahu, Nirmal Kumar Ganguly, Pradip Chakraborti, Mandaville Gourie-Devi, Vibha Taneja

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular neurobiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
10.6field-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

71 citing papers in PubMed, 91 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Junctions in Jeopardy: the neuromuscular junction is a selective pathological target in Charcot-Marie-Tooth disease.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
    Review
  8. Article
  9. Article
  10. Impact of Oxidative Stress-Driven Ferroptosis in Neurodegeneration.International journal of molecular sciences · 2026
    Review
  11. Review of the Pathology of Muscle in Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2026
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. The Neuromuscular Junction: A Shared Vulnerability in Aging and Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Review
  19. Article
  20. Article

11 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

8 authors at 4 institutions in 2 countries.

Sagar VermaDepartment of Research, Sir Ganga Ram Hospital, Delhi, India.
Shiffali KhuranaDepartment of Research, Sir Ganga Ram Hospital, Delhi, India.
Abhishek VatsDepartment of Ophthalmology, School of Medicine, University of Pittsburgh, Pittsburgh, PA, USA.
Bandana SahuDepartment of Research, Sir Ganga Ram Hospital, Delhi, India.
Nirmal Kumar GangulyDepartment of Research, Sir Ganga Ram Hospital, Delhi, India.
Pradip ChakrabortiDepartment of Biotechnology, Jamia Hamdard, Delhi, India.
Mandaville Gourie-DeviDepartment of Neurophysiology, Sir Ganga Ram Hospital, Delhi, India.
Vibha TanejaDepartment of Research, Sir Ganga Ram Hospital, Delhi, India. vibha.taneja@sgrh.com.ORCID http://orcid.org/0000-0001-5457-9992
Sir Ganga Ram Hospital · INJamia Hamdard · INUniversity of Delhi · INUniversity of Pittsburgh · US

Funding

council of scientific and industrial research, india 09/591(0150)/2018-EMR-Iindian council of medical research 3/1/3/JRF-2012/HRDindian council of medical research BIC/05 (09)/Indo-Russian/2016indian council of medical research BMS/Adhoc/BIOCHEM/2015-0430
6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) is a fatal neurological disorder characterized by progressive degeneration of motor neurons leading to skeletal muscle denervation. Earlier studies have shown that motor neuron degeneration begins in motor cortex and descends to the neuromuscular junction (NMJ) in a dying forward fashion. However, accumulating evidences support that ALS is a distal axonopathy where early pathological changes occur at the NMJ, prior to onset of clinical symptoms and propagates towards the motor neuron cell body supporting "dying back" hypothesis. Despite several evidences, series of events triggering NMJ disassembly in ALS are still obscure. Neuromuscular junction is a specialized tripartite chemical synapse which involves a well-coordinated communication among the presynaptic motor neuron, postsynaptic skeletal muscle, and terminal Schwann cells. This review provides comprehensive insight into the role of NMJ in ALS pathogenesis. We have emphasized the molecular alterations in cellular components of NMJ leading to loss of effective neuromuscular transmission in ALS. Further, we provide a preview into research involved in exploring NMJ as potential target for designing effective therapies for ALS.

Indexed as

Amyotrophic Lateral SclerosisHumansMotor NeuronsMuscle, SkeletalNeuromuscular JunctionSuperoxide Dismutase-1SynapsesSuperoxide Dismutase-1Amyotrophic lateral sclerosisDying backMotor neuronNeuromuscular junctionSkeletal muscleTerminal Schwann cells

Identifiers

PMID34997540
OpenAlexW4205177830

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.