Synofzik Matthis, Smets Katrien, Mallaret Martial, Di Bella Daniela, Gallenmüller Constanze, Baets Jonathan, Schulze Martin, Magri Stefania, Sarto Elisa, Mustafa Mona, Deconinck Tine, Haack Tobias, Züchner Stephan, Gonzalez Michael, Timmann Dagmar, Stendel Claudia, Klopstock Thomas, Durr Alexandra, Tranchant Christine, Sturm Marc, Hamza Wahiba, Nanetti Lorenzo, Mariotti Caterina, Koenig Michel, Schöls Ludger, Schüle Rebecca, de Jonghe Peter, Anheim Mathieu, Taroni Franco, Bauer Peter
Department of Neurodegenerative Diseases, Hertie-Institute for Clinical Brain Research, University of Tübingen, Germany German Research Center for Neurodegenerative Diseases (DZNE), University of Tübingen, Germany
Neurogenetics Group, Department of Molecular Genetics, University of Antwerp, VIB Belgium Department of Neurology, Antwerp University Hospital, Belgium Laboratory of Neurogenetics, Institute Born-Bunge, University of Antwerp, Belgium.
Brain. 2016 May;139(Pt 5):1378-93. doi: 10.1093/brain/aww079. Epub 2016 Apr 17.
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.
据报道,突触核被膜蛋白1(SYNE1)基因突变会导致一种相对单纯、进展缓慢的小脑隐性共济失调,这种疾病主要在加拿大魁北克被发现。我们结合下一代测序技术和深度表型分析(临床检查、磁共振成像、正电子发射断层扫描、肌肉组织学),在对来自欧洲七个中心的434名非加拿大索引患者进行的筛查中,确定了SYNE1的发生率、表型谱和基因谱。通过全外显子组测序或靶向基因panel测序对患者进行筛查,发现了23个携带隐性截短SYNE1突变的无关家庭(23/434 = 5.3%)。在这些家庭中,共鉴定出35种不同的突变,其中34种此前未与人类疾病相关联。虽然只有5/26例患者(19%)表现出轻度进展性单纯小脑共济失调的经典SYNE1表型,但21/26例(81%)表现出其他复杂特征,其中15/26例(58%)具有运动神经元特征。在3例患者中,呼吸功能障碍是一种早发性多系统神经肌肉表型的一部分,伴有智力障碍,其中1例在36岁时过早死亡。正电子发射断层扫描成像证实了脑干等小脑外区域的代谢减低。肌肉活检可靠地显示SYNE1染色严重减少或缺失,表明其有可能作为潜在SYNE1突变的非基因指标。我们的研究结果呈现了加拿大以外最大规模的SYNE1患者和突变的系统性系列,修正了认为SYNE1共济失调主要导致相对单纯的小脑隐性共济失调且主要局限于魁北克的观点。相反,具有广泛小脑外神经和非神经功能障碍的复杂表型很常见,尤其是运动神经元和脑干功能障碍。这种多系统神经退行性疾病的病程可能是致命的,包括因呼吸功能障碍导致的过早死亡。SYNE1的相对发生率约为5%,是全球较常见的隐性共济失调之一。