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Cited by 131

The DOI matches its Crossref record; 33 of the 33 references it cites were found in a registry or an index.

Muscle histone deacetylase 4 upregulation in amyotrophic lateral sclerosis: potential role in reinnervation ability and disease progression

Bruneteau, Gaëlle, Simonet, Thomas, Bauché, Stéphanie, Mandjee, Nathalie, Malfatti, Edoardo, Girard, Emmanuelle, Tanguy, Marie-Laure, Behin, Anthony, Khiami, Frédéric, Sariali, Elhadi, Hell-Remy, Caroline, Salachas, François, Pradat, Pierre-François, Fournier, Emmanuel, Lacomblez, Lucette, Koenig, Jeanine, Romero, Norma Beatriz, Fontaine, Bertrand, Meininger, Vincent, Schaeffer, Laurent, Hantaï, Daniel·2013·Brain
DOI 10.1093/brain/awt164
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Abstract

Amyotrophic lateral sclerosis is a typically rapidly progressive neurodegenerative disorder affecting motor neurons leading to progressive muscle paralysis and death, usually from respiratory failure, in 3-5 years. Some patients have slow disease progression and prolonged survival, but the underlying mechanisms remain poorly understood. Riluzole, the only approved treatment, only modestly prolongs survival and has no effect on muscle function. In the early phase of the disease, motor neuron loss is initially compensated for by collateral reinnervation, but over time this compensation fails, leading to progressive muscle wasting. The crucial role of muscle histone deacetylase 4 and its regulator microRNA-206 in compensatory reinnervation and disease progression was recently suggested in a mouse model of amyotrophic lateral sclerosis (transgenic mice carrying human mutations in the superoxide dismutase gene). Here, we sought to investigate whether the microRNA-206-histone deacetylase 4 pathway plays a role in muscle compensatory reinnervation in patients with amyotrophic lateral sclerosis and thus contributes to disease outcome differences. We studied muscle reinnervation using high-resolution confocal imaging of neuromuscular junctions in muscle samples obtained from 11 patients with amyotrophic lateral sclerosis, including five long-term survivors. We showed that the proportion of reinnervated neuromuscular junctions was significantly higher in long-term survivors than in pat…

Overview

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Crossref · 10.1093/brain/awt164

Cites

33 of 33 references verified0 citation errors · 0 not checkable

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Citations

Cites

Research works printed but not linked: 1

  1. Cöers, 1964, Morphologie de la jonction neuromusculaire, Arch Biol (Liège), 75, 905

Cited by

See all 131

Metadata

Authors
Bruneteau, G., Simonet, T., Bauché, S., Mandjee, N., Malfatti, E., Girard, E., Tanguy, M.-L., Behin, A., Khiami, F., Sariali, E., Hell-Remy, C., Salachas, F., Pradat, P.-F., Fournier, E., Lacomblez, L., Koenig, J., Romero, N. B., Fontaine, B., Meininger, V., Schaeffer, L., & Hantaï, D.
Venue
Brain
Publisher
Oxford University Press (OUP)
Published
2013-07-03
Volume
136
Issue
8
Pages
2359-2368
ISSN
  • 1460-2156
  • 0006-8950
DOI
10.1093/brain/awt164
Cited by
131
References
33
Language
en

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.