An SPG7 mutation as a novel cause of monogenic progressive muscular atrophy.


Journal

Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
ISSN: 1590-3478
Titre abrégé: Neurol Sci
Pays: Italy
ID NLM: 100959175

Informations de publication

Date de publication:
Sep 2023
Historique:
received: 15 03 2023
accepted: 17 05 2023
medline: 11 8 2023
pubmed: 22 5 2023
entrez: 22 5 2023
Statut: ppublish

Résumé

Progressive muscular atrophy (PMA) is a rare adult-onset neurological disease that is characterized by isolated lower motor neuron degeneration. While it is still disputable whether PMA is a subtype of amyotrophic lateral sclerosis (ALS) or an isolated disorder, it is well-established as a clinically defined entity. About 5% of PMA cases are monogenic, and the implicated genes largely overlap with those causing monogenic ALS. Here we describe a 68-year-old female patient with progressive and asymmetric upper-limb weakness throughout an 18-month period, with muscle atrophy, dysphagia and slurring of speech. The lower limbs were unaffected, and there was no sign of upper motor neuron dysfunction. Comprehensive genetic testing for single nucleotide and copy-number variants revealed a pathogenic monoallelic variant c.1529C>T, p.(Ala510Val) in the SPG7 gene. Pathogenic biallelic SPG7 variants have been originally associated with hereditary spastic paraplegia, but other phenotypes are nowadays known to be linked to these variants, such as ALS. However, there is no report of this (or any) other SPG7 variant in association with PMA, whether it progressed to ALS or not. In conclusion, we present the first known case of PMA associated with a monoallelic SPG7 mutation.

Sections du résumé

BACKGROUND BACKGROUND
Progressive muscular atrophy (PMA) is a rare adult-onset neurological disease that is characterized by isolated lower motor neuron degeneration. While it is still disputable whether PMA is a subtype of amyotrophic lateral sclerosis (ALS) or an isolated disorder, it is well-established as a clinically defined entity. About 5% of PMA cases are monogenic, and the implicated genes largely overlap with those causing monogenic ALS.
CASE DESCRIPTION METHODS
Here we describe a 68-year-old female patient with progressive and asymmetric upper-limb weakness throughout an 18-month period, with muscle atrophy, dysphagia and slurring of speech. The lower limbs were unaffected, and there was no sign of upper motor neuron dysfunction. Comprehensive genetic testing for single nucleotide and copy-number variants revealed a pathogenic monoallelic variant c.1529C>T, p.(Ala510Val) in the SPG7 gene.
DISCUSSION CONCLUSIONS
Pathogenic biallelic SPG7 variants have been originally associated with hereditary spastic paraplegia, but other phenotypes are nowadays known to be linked to these variants, such as ALS. However, there is no report of this (or any) other SPG7 variant in association with PMA, whether it progressed to ALS or not. In conclusion, we present the first known case of PMA associated with a monoallelic SPG7 mutation.

Identifiants

pubmed: 37213040
doi: 10.1007/s10072-023-06867-w
pii: 10.1007/s10072-023-06867-w
doi:

Substances chimiques

SPG7 protein, human EC 3.4.24.-
ATPases Associated with Diverse Cellular Activities EC 3.6.4.-
Metalloendopeptidases EC 3.4.24.-

Types de publication

Case Reports Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

3303-3305

Informations de copyright

© 2023. Fondazione Società Italiana di Neurologia.

Références

Patten SA, Armstrong GAB, Lissouba A et al (2014) Fishing for causes and cures of motor neuron disorders. Dis Model Mech 7:799–809. https://doi.org/10.1242/dmm.015719
doi: 10.1242/dmm.015719 pubmed: 24973750 pmcid: 4073270
Liewluck T, Saperstein DS (2015) Progressive muscular atrophy. Neurol Clin 33:761–773. https://doi.org/10.1016/j.ncl.2015.07.005
doi: 10.1016/j.ncl.2015.07.005 pubmed: 26515620
Siddique N, Siddique T (1993) In: Adam MP, Everman DB, Mirzaa GM et al (eds) Amyotrophic lateral sclerosis overview, Seattle (WA)
Casari G, De Fusco M, Ciarmatori S et al (1998) Spastic paraplegia and OXPHOS impairment caused by mutations in paraplegin, a nuclear-encoded mitochondrial metalloprotease. Cell 93:973–983. https://doi.org/10.1016/s0092-8674(00)81203-9
doi: 10.1016/s0092-8674(00)81203-9 pubmed: 9635427
Casari G, Marconi R (1993) Spastic paraplegia 7. In: Adam MP, Everman DB, Mirzaa GM et al (eds) Gene Reviews, Seattle (WA)
Osmanovic A, Widjaja M, Förster A et al (2020) SPG7 mutations in amyotrophic lateral sclerosis: a genetic link to hereditary spastic paraplegia. J Neurol 267:2732–2743. https://doi.org/10.1007/s00415-020-09861-w
doi: 10.1007/s00415-020-09861-w pubmed: 32447552 pmcid: 7419373
Sánchez-Ferrero E, Coto E, Beetz C et al (2013) SPG7 mutational screening in spastic paraplegia patients supports a dominant effect for some mutations and a pathogenic role for p.A510V. Clin Genet 83:257–262. https://doi.org/10.1111/j.1399-0004.2012.01896.x
doi: 10.1111/j.1399-0004.2012.01896.x pubmed: 22571692
Estiar MA, Yu E, Haj Salem I et al (2021) Evidence for non-Mendelian inheritance in spastic paraplegia 7. Mov Disord 36:1664–1675. https://doi.org/10.1002/mds.28528
doi: 10.1002/mds.28528 pubmed: 33598982
Krüger S, Battke F, Sprecher A et al (2016) Rare variants in neurodegeneration associated genes revealed by targeted panel sequencing in a German ALS cohort. Front Mol Neurosci 9:92. https://doi.org/10.3389/fnmol.2016.00092
doi: 10.3389/fnmol.2016.00092 pubmed: 27790088 pmcid: 5061735
Garton FC, Benyamin B, Zhao Q et al (2017) Whole exome sequencing and DNA methylation analysis in a clinical amyotrophic lateral sclerosis cohort. Mol Genet genomic Med 5:418–428. https://doi.org/10.1002/mgg3.302
doi: 10.1002/mgg3.302 pubmed: 28717666 pmcid: 5511806

Auteurs

Ângela Pereira (Â)

Centro Materno-Infantil do Norte, Centro Hospital Universitário de Santo António, Porto, Portugal.
Hospital de Braga, Braga, Portugal.

Nataliya Tkachenko (N)

Centro de Genética Médica Doutor Jacinto Magalhães (CGM), Centro Hospitalar Universitário de Santo António, Porto, Portugal.
Unit for Multidisciplinary Research in Biomedicine, Abel Salazar Biomedical Sciences Institute, Porto University, Porto, Portugal.

Ana Maria Fortuna (AM)

Centro de Genética Médica Doutor Jacinto Magalhães (CGM), Centro Hospitalar Universitário de Santo António, Porto, Portugal.
Unit for Multidisciplinary Research in Biomedicine, Abel Salazar Biomedical Sciences Institute, Porto University, Porto, Portugal.

Isabel Alonso (I)

Genetyca-ICM, Atrys, Porto, Portugal.

Márcio Cardoso (M)

Corino de Andrade Unit, Centro Hospitalar Universitário de Santo António, Porto, Portugal.

Jorge Diogo Da Silva (JD)

Centro de Genética Médica Doutor Jacinto Magalhães (CGM), Centro Hospitalar Universitário de Santo António, Porto, Portugal. jorge.diogo.silva@chporto.min-saude.pt.
Unit for Multidisciplinary Research in Biomedicine, Abel Salazar Biomedical Sciences Institute, Porto University, Porto, Portugal. jorge.diogo.silva@chporto.min-saude.pt.
Life and Health Sciences Research Institute (ICVS), School of Medicine, University of Minho, Braga, Portugal. jorge.diogo.silva@chporto.min-saude.pt.
ICVS/3B's-PT Government Associate Laboratory, Braga/Guimarães, Portugal. jorge.diogo.silva@chporto.min-saude.pt.

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