Myopathic changes caused by protein aggregates in adult-onset spinal muscular atrophy.


Journal

Neuropathology : official journal of the Japanese Society of Neuropathology
ISSN: 1440-1789
Titre abrégé: Neuropathology
Pays: Australia
ID NLM: 9606526

Informations de publication

Date de publication:
Oct 2023
Historique:
revised: 12 02 2023
received: 16 01 2023
accepted: 17 02 2023
medline: 23 10 2023
pubmed: 4 3 2023
entrez: 3 3 2023
Statut: ppublish

Résumé

Spinal muscular atrophy (SMA), an autosomal-recessive lower motor neuron disease, causes progressive proximal muscle waste and weakness. It remains unclear whether myopathic changes are involved in pathogenesis. We encountered a patient with adult-onset SMA caused by a homozygous deletion in exon 7 of the survival motor neuron 1 (SMN1) gene who had had four copies of SMN2 exon 7. Muscle biopsy showed neurogenic features of groups of atrophic fibers, fiber-type grouping, and pyknotic nuclear clumps associated with fibers with rimmed vacuoles. Immunohistochemistry revealed sarcoplasmic aggregates of phosphorylated TDP-43 and p62 but not SMN. This study demonstrated myopathic changes with the accumulation of phosphorylated p62 and TDP-43 in the muscles of a patient with SMA, suggesting that abnormal protein aggregation may be involved in myopathic pathology.

Identifiants

pubmed: 36864825
doi: 10.1111/neup.12901
doi:

Substances chimiques

Protein Aggregates 0
DNA-Binding Proteins 0

Types de publication

Case Reports

Langues

eng

Sous-ensembles de citation

IM

Pagination

408-412

Subventions

Organisme : Japan Society for the Promotion of Science
Organisme : Ministry of Health, Labour and Welfare

Informations de copyright

© 2023 Japanese Society of Neuropathology.

Références

Hamilton G, Gillingwater TH. Spinal muscular atrophy: Going beyond the motor neuron. Trends Mol Med 2013; 19: 40-50.
Nash LA, Burns JK, Chardon JW et al. Spinal muscular atrophy: More than a disease of motor neurons? Curr Mol Med 2016; 16: 779-792.
Souza PVS, Pinto W, Ricarte A et al. Clinical and radiological profile of patients with spinal muscular atrophy type 4. Eur J Neurol 2021; 28: 609-619.
Brogna C, Cristiano L, Verdolotti T et al. MRI patterns of muscle involvement in type 2 and 3 spinal muscular atrophy patients. J Neurol 2020; 267: 898-912.
Phillips BA, Cala LA, Thickbroom GW, Melsom A, Zilko PJ, Mastaglia FL. Patterns of muscle involvement in inclusion body myositis: Clinical and magnetic resonance imaging study. Muscle Nerve 2001; 24: 1526-1534.
Jokela M, Huovinen S, Raheem O et al. Distinct muscle biopsy findings in genetically defined adult-onset motor neuron disorders. PLoS One 2016; 11: e0151376.
Madigan NN, Tracy JA, Litchy WJ et al. A tropomyosin-receptor kinase-fused gene mutation associates with vacuolar myopathy. Neurol Genet 2018; 4: e287.
Yamashita S, Kimura E, Zhang Z et al. Muscle pathology of hereditary motor and sensory neuropathy with proximal dominant involvement with TFG mutation. Muscle Nerve 2019; 60: 739-744.
Rodriguez-Muela N, Parkhitko A, Grass T et al. Blocking p62-dependent SMN degradation ameliorates spinal muscular atrophy disease phenotypes. J Clin Invest 2018; 128: 3008-3023.
Kim JK, Jha NN, Feng Z et al. Muscle-specific SMN reduction reveals motor neuron-independent disease in spinal muscular atrophy models. J Clin Invest 2020; 130: 1271-1287.

Auteurs

Satoshi Yamashita (S)

Department of Neurology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Department of Neurology, International University of Health and Welfare Narita Hospital, Narita, Japan.

Akihito Nagatoshi (A)

Department of Neurology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Department of Neurology, National Hospital Organization Kumamotominami National Hospital, Uki, Japan.

Yosuke Takeuchi (Y)

Department of Neurology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.

Ichizo Nishino (I)

Department of Neuromuscular Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Japan.

Mitsuharu Ueda (M)

Department of Neurology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.

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Classifications MeSH