Preservation of masseter muscle until the end stage in the SOD1G93A mouse model for ALS

Kawata, Sou; Seki, Soju; Nishiura, Akira; Kitaoka, Yoshihiro; Iwamori, Kanako; Fukada, So-Ichiro; Kogo, Mikihiko; Tanaka, Susumu

doi:https://doi.org/10.1038/s41598-024-74669-x

Preservation of masseter muscle until the end stage in the SOD1G93A mouse model for ALS

Kawata, Sou; Seki, Soju; Nishiura, Akira et al.

Scientific Reports, 2024, 14, 24279

アクセス数:998件（2025-08-15 19:12 集計）

固定URL: https://hdl.handle.net/11094/98551

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タイトル	Preservation of masseter muscle until the end stage in the SOD1G93A mouse model for ALS
著者	著者名 Kawata, Sou
	NRID 1000060755081 1000060755081 researchmap permalink sojuseki sojuseki 著者名 Seki, Soju
	著者名 Nishiura, Akira
	著者名 Kitaoka, Yoshihiro
	著者名 Iwamori, Kanako
	NRID 1000020432445 1000020432445 ORCID 0000-0003-4051-5108 0000-0003-4051-5108 researchmap permalink mdx mdx Scopus Author ID 56020906000 56020906000 著者名 Fukada, So-Ichiro
	NRID 1000020205371 1000020205371 ORCID 0000-0002-4556-2491 0000-0002-4556-2491 researchmap permalink 4321Kogo2 4321Kogo2 Scopus Author ID 7003762492 7003762492 著者名 Kogo, Mikihiko
	NRID 1000000367541 1000000367541 ORCID 0000-0002-0306-3627 0000-0002-0306-3627 researchmap permalink mes5 mes5 Scopus Author ID 56395750500 56395750500 著者名 Tanaka, Susumu
キーワード等	Amyotrophic lateral sclerosis
	Gastrocnemius muscle
	Masseter muscles
	Satellite cells
	Voluntary muscle control
内容	Kawata S., Seki S., Nishiura A., et al. Preservation of masseter muscle until the end stage in the SOD1G93A mouse model for ALS. Scientific Reports 14, 24279 (2024); https://doi.org/10.1038/s41598-024-74669-x.
抄録	Amyotrophic lateral sclerosis (ALS) progressively impairs motor neurons, leading to muscle weakness and loss of voluntary muscle control. This study compared the effects of SOD1 mutation on masticatory and limb muscles from disease onset to death in ALS model mice. Notably, limb muscles begin to atrophy soon after ALS-like phenotype appear, whereas masticatory muscles maintain their volume and function in later stages. Our analysis showed that, unlike limb muscles, masticatory muscles retain their normal structure and cell makeup throughout most of the disease course. We found an increase in the number of muscle satellite cells (SCs), which are essential for muscle repair, in masticatory muscles. In addition, we observed no reduction in the number of muscle nuclei and no muscle fibre-type switching in masticatory muscles. This indicates that masticatory muscles have a higher resistance to ALS-related damage than limb muscles, likely because of differences in cell composition and repair mechanisms. Understanding why masticatory muscles are less affected by ALS could lead to the development of new treatments. This study highlights the importance of studying different muscle groups in ALS to clarify disease aetiology and mechanisms.
出版者	Nature Research
収録物名	Scientific Reports
巻(号)	14
ページ	24279
刊行年月	2024-10-16
言語	英語
ハンドルURL	https://hdl.handle.net/11094/98551
eISSN	20452322
関連情報 (isIdenticalTo)	DOI (出版社版) https://doi.org/10.1038/s41598-024-74669-x
アクセス権	open access
権利情報	This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
出版タイプ	Version of Record
カテゴリ	学術雑誌論文 Journal Article

資源タイプ	学術雑誌論文
ローカル資源タイプ	学術雑誌論文
DCTERMS.bibliographicCitation	Scientific Reports. 2024, 14, p. 24279
DC.title	Preservation of masseter muscle until the end stage in the SOD1G93A mouse model for ALS
DC.creator	Kawata, Sou
	Seki, Soju
	Nishiura, Akira
	Kitaoka, Yoshihiro
	Iwamori, Kanako
	Fukada, So-Ichiro
	Kogo, Mikihiko
	Tanaka, Susumu
DC.publisher	Nature Research
DC.language' scheme='DCTERMS.RFC1766	英語
DCTERMS.issued' scheme='DCTERMS.W3CDTF	2024-10-16
DC.identifier	https://doi.org/10.1038/s41598-024-74669-x
DC.subject	Amyotrophic lateral sclerosis
	Gastrocnemius muscle
	Masseter muscles
	Satellite cells
	Voluntary muscle control
DC.description	Kawata S., Seki S., Nishiura A., et al. Preservation of masseter muscle until the end stage in the SOD1G93A mouse model for ALS. Scientific Reports 14, 24279 (2024); https://doi.org/10.1038/s41598-024-74669-x.
DCTERMS.abstract	Amyotrophic lateral sclerosis (ALS) progressively impairs motor neurons, leading to muscle weakness and loss of voluntary muscle control. This study compared the effects of SOD1 mutation on masticatory and limb muscles from disease onset to death in ALS model mice. Notably, limb muscles begin to atrophy soon after ALS-like phenotype appear, whereas masticatory muscles maintain their volume and function in later stages. Our analysis showed that, unlike limb muscles, masticatory muscles retain their normal structure and cell makeup throughout most of the disease course. We found an increase in the number of muscle satellite cells (SCs), which are essential for muscle repair, in masticatory muscles. In addition, we observed no reduction in the number of muscle nuclei and no muscle fibre-type switching in masticatory muscles. This indicates that masticatory muscles have a higher resistance to ALS-related damage than limb muscles, likely because of differences in cell composition and repair mechanisms. Understanding why masticatory muscles are less affected by ALS could lead to the development of new treatments. This study highlights the importance of studying different muscle groups in ALS to clarify disease aetiology and mechanisms.
DC.rights	This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
DC.format	98551
citation_title	Preservation of masseter muscle until the end stage in the SOD1G93A mouse model for ALS
citation_author	Kawata, Sou
	Seki, Soju
	Nishiura, Akira
	Kitaoka, Yoshihiro
	Iwamori, Kanako
	Fukada, So-Ichiro
	Kogo, Mikihiko
	Tanaka, Susumu
citation_publisher	Nature Research
citation_language	英語
citation_date	2024-10-16
citation_journal_title	Scientific Reports
citation_volume	14
citation_firstpage	24279
citation_doi	https://doi.org/10.1038/s41598-024-74669-x
citation_public_url	https://hdl.handle.net/11094/98551

Preservation of masseter muscle until the end stage in the SOD1G93A mouse model for ALS

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