Skeletal muscle in amyotrophic lateral sclerosis.
denervation
energy metabolism
mouse models
neuromuscular junction
neurophysiology
Journal
Brain : a journal of neurology
ISSN: 1460-2156
Titre abrégé: Brain
Pays: England
ID NLM: 0372537
Informations de publication
Date de publication:
02 11 2023
02 11 2023
Historique:
received:
30
03
2023
revised:
16
05
2023
accepted:
30
05
2023
medline:
9
11
2023
pubmed:
16
6
2023
entrez:
16
6
2023
Statut:
ppublish
Résumé
Amyotrophic lateral sclerosis (ALS), the major adult-onset motor neuron disease, has been viewed almost exclusively as a disease of upper and lower motor neurons, with muscle changes interpreted as a consequence of the progressive loss of motor neurons and neuromuscular junctions. This has led to the prevailing view that the involvement of muscle in ALS is only secondary to motor neuron loss. Skeletal muscle and motor neurons reciprocally influence their respective development and constitute a single functional unit. In ALS, multiple studies indicate that skeletal muscle dysfunction might contribute to progressive muscle weakness, as well as to the final demise of neuromuscular junctions and motor neurons. Furthermore, skeletal muscle has been shown to participate in disease pathogenesis of several monogenic diseases closely related to ALS. Here, we move the narrative towards a better appreciation of muscle as a contributor of disease in ALS. We review the various potential roles of skeletal muscle cells in ALS, from passive bystanders to active players in ALS pathophysiology. We also compare ALS to other motor neuron diseases and draw perspectives for future research and treatment.
Identifiants
pubmed: 37327376
pii: 7199715
doi: 10.1093/brain/awad202
pmc: PMC10629757
doi:
Types de publication
Review
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
4425-4436Informations de copyright
© The Author(s) 2023. Published by Oxford University Press on behalf of the Guarantors of Brain.
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