Literature DB >> 27086870

SYNE1 ataxia is a common recessive ataxia with major non-cerebellar features: a large multi-centre study.

Matthis Synofzik1, Katrien Smets2, Martial Mallaret3, Daniela Di Bella4, Constanze Gallenmüller5, Jonathan Baets2, Martin Schulze6, Stefania Magri4, Elisa Sarto4, Mona Mustafa7, Tine Deconinck8, Tobias Haack9, Stephan Züchner10, Michael Gonzalez10, Dagmar Timmann11, Claudia Stendel12, Thomas Klopstock5, Alexandra Durr13, Christine Tranchant3, Marc Sturm6, Wahiba Hamza14, Lorenzo Nanetti4, Caterina Mariotti4, Michel Koenig15, Ludger Schöls16, Rebecca Schüle17, Peter de Jonghe2, Mathieu Anheim18, Franco Taroni4, Peter Bauer6.   

Abstract

Mutations in the synaptic nuclear envelope protein 1 (SYNE1) gene have been reported to cause a relatively pure, slowly progressive cerebellar recessive ataxia mostly identified in Quebec, Canada. Combining next-generation sequencing techniques and deep-phenotyping (clinics, magnetic resonance imaging, positron emission tomography, muscle histology), we here established the frequency, phenotypic spectrum and genetic spectrum of SYNE1 in a screening of 434 non-Canadian index patients from seven centres across Europe. Patients were screened by whole-exome sequencing or targeted panel sequencing, yielding 23 unrelated families with recessive truncating SYNE1 mutations (23/434 = 5.3%). In these families, 35 different mutations were identified, 34 of them not previously linked to human disease. While only 5/26 patients (19%) showed the classical SYNE1 phenotype of mildly progressive pure cerebellar ataxia, 21/26 (81%) exhibited additional complicating features, including motor neuron features in 15/26 (58%). In three patients, respiratory dysfunction was part of an early-onset multisystemic neuromuscular phenotype with mental retardation, leading to premature death at age 36 years in one of them. Positron emission tomography imaging confirmed hypometabolism in extra-cerebellar regions such as the brainstem. Muscle biopsy reliably showed severely reduced or absent SYNE1 staining, indicating its potential use as a non-genetic indicator for underlying SYNE1 mutations. Our findings, which present the largest systematic series of SYNE1 patients and mutations outside Canada, revise the view that SYNE1 ataxia causes mainly a relatively pure cerebellar recessive ataxia and that it is largely limited to Quebec. Instead, complex phenotypes with a wide range of extra-cerebellar neurological and non-neurological dysfunctions are frequent, including in particular motor neuron and brainstem dysfunction. The disease course in this multisystemic neurodegenerative disease can be fatal, including premature death due to respiratory dysfunction. With a relative frequency of ∼5%, SYNE1 is one of the more common recessive ataxias worldwide.
© The Author (2016). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oup.com.

Entities:  

Keywords:  Nesprin 1; ataxia; genetics; hereditary spastic paraplegia; motor neuron disease

Mesh:

Substances:

Year:  2016        PMID: 27086870      PMCID: PMC6363274          DOI: 10.1093/brain/aww079

Source DB:  PubMed          Journal:  Brain        ISSN: 0006-8950            Impact factor:   13.501


  35 in total

1.  ANO10 mutational screening in recessive ataxia: genetic findings and refinement of the clinical phenotype.

Authors:  Lorenzo Nanetti; Elisa Sarto; Anna Castaldo; Stefania Magri; Alessia Mongelli; Davide Rossi Sebastiano; Laura Canafoglia; Marina Grisoli; Chiara Malaguti; Francesca Rivieri; Maria Chiara D'Amico; Daniela Di Bella; Silvana Franceschetti; Caterina Mariotti; Franco Taroni
Journal:  J Neurol       Date:  2018-12-04       Impact factor: 4.849

2.  Pathogenic mutations in genes encoding nuclear envelope proteins and defective nucleocytoplasmic connections.

Authors:  Cecilia Östlund; Wakam Chang; Gregg G Gundersen; Howard J Worman
Journal:  Exp Biol Med (Maywood)       Date:  2019-07-12

3.  SPG7: The Great Imitator of MSA-C Within the ILOCAs.

Authors:  Paula Salgado; Anna Latorre; Claudia Del Gamba; Elisa Menozzi; Bettina Balint; Kailash P Bhatia
Journal:  Mov Disord Clin Pract       Date:  2018-12-06

Review 4.  Overcoming the divide between ataxias and spastic paraplegias: Shared phenotypes, genes, and pathways.

Authors:  Matthis Synofzik; Rebecca Schüle
Journal:  Mov Disord       Date:  2017-02-14       Impact factor: 10.338

5.  Validation of a clinical practice-based algorithm for the diagnosis of autosomal recessive cerebellar ataxias based on NGS identified cases.

Authors:  Martial Mallaret; Mathilde Renaud; Claire Redin; Nathalie Drouot; Jean Muller; Francois Severac; Jean Louis Mandel; Wahiba Hamza; Traki Benhassine; Lamia Ali-Pacha; Meriem Tazir; Alexandra Durr; Marie-Lorraine Monin; Cyril Mignot; Perrine Charles; Lionel Van Maldergem; Ludivine Chamard; Christel Thauvin-Robinet; Vincent Laugel; Lydie Burglen; Patrick Calvas; Marie-Céline Fleury; Christine Tranchant; Mathieu Anheim; Michel Koenig
Journal:  J Neurol       Date:  2016-05-03       Impact factor: 4.849

Review 6.  Clinical application of next generation sequencing in hereditary spinocerebellar ataxia: increasing the diagnostic yield and broadening the ataxia-spasticity spectrum. A retrospective analysis.

Authors:  Daniele Galatolo; Alessandra Tessa; Alessandro Filla; Filippo M Santorelli
Journal:  Neurogenetics       Date:  2017-12-06       Impact factor: 2.660

7.  Multiple Isoforms of Nesprin1 Are Integral Components of Ciliary Rootlets.

Authors:  Chloe Potter; Wanqiu Zhu; David Razafsky; Philip Ruzycki; Alexander V Kolesnikov; Teresa Doggett; Vladimir J Kefalov; Ewelina Betleja; Moe R Mahjoub; Didier Hodzic
Journal:  Curr Biol       Date:  2017-06-15       Impact factor: 10.834

8.  The KASH-containing isoform of Nesprin1 giant associates with ciliary rootlets of ependymal cells.

Authors:  C Potter; D Razafsky; D Wozniak; M Casey; S Penrose; X Ge; M R Mahjoub; D Hodzic
Journal:  Neurobiol Dis       Date:  2018-04-06       Impact factor: 5.996

9.  Loss-of-function mutations in the ATP13A2/PARK9 gene cause complicated hereditary spastic paraplegia (SPG78).

Authors:  Alejandro Estrada-Cuzcano; Shaun Martin; Teodora Chamova; Matthis Synofzik; Dagmar Timmann; Tine Holemans; Albena Andreeva; Jennifer Reichbauer; Riet De Rycke; Dae-In Chang; Sarah van Veen; Jean Samuel; Ludger Schöls; Thorsten Pöppel; Danny Mollerup Sørensen; Bob Asselbergh; Christine Klein; Stephan Zuchner; Albena Jordanova; Peter Vangheluwe; Ivailo Tournev; Rebecca Schüle
Journal:  Brain       Date:  2017-02       Impact factor: 13.501

10.  Multisystemic SYNE1 ataxia: confirming the high frequency and extending the mutational and phenotypic spectrum.

Authors:  Inès Mademan; Florian Harmuth; Ilaria Giordano; Dagmar Timmann; Stefania Magri; Tine Deconinck; Jens Claaßen; Daniel Jokisch; Gencer Genc; Daniela Di Bella; Silvia Romito; Rebecca Schüle; Stephan Züchner; Franco Taroni; Thomas Klockgether; Ludger Schöls; Peter De Jonghe; Peter Bauer; Eoa Consortium; Jonathan Baets; Matthis Synofzik
Journal:  Brain       Date:  2016-05-19       Impact factor: 13.501

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