From the Department of Molecular Neuroscience (G.C., N.W.W.), and Sobell Department of Motor Neuroscience and Movement Disorders (M.S., K.P.B.), UCL Institute of Neurology, Queen Square, London, UK; Neurology Centre and Research (M.D.M.), Kolhapur, India; Department of Neurology (S.A.S.), University of Kiel, Germany; Movement Disorders Clinic (M.S.), Second Department of Neurology, Attiko Hospital, University of Athens, Greece; and Neurology Clinic (M.S.), Philipps University, Marburg, Germany.
Neurology. 2013 Sep 24;81(13):1148-51. doi: 10.1212/WNL.0b013e3182a55fa2. Epub 2013 Aug 14.
To identify the cause of cervical dopa-responsive dystonia (DRD) in a Muslim Indian family inherited in an apparently autosomal recessive fashion, as previously described in this journal.
Previous testing for mutations in the genes known to cause DRD (GCH1, TH, and SPR) had been negative. Whole exome sequencing was performed on all 3 affected individuals for whom DNA was available to identify potentially pathogenic shared variants. Genotyping data obtained for all 3 affected individuals using the OmniExpress single nucleotide polymorphism chip (Illumina, San Diego, CA) were used to perform linkage analysis, autozygosity mapping, and copy number variation analysis. Sanger sequencing was used to confirm all variants.
After filtering of the variants, exome sequencing revealed 2 genes harboring potentially pathogenic compound heterozygous variants (ATM and LRRC16A). Of these, the variants in ATM segregated perfectly with the cervical DRD. Both mutations detected in ATM have been shown to be pathogenic, and α-fetoprotein, a marker of ataxia telangiectasia, was increased in all affected individuals.
Biallelic mutations in ATM can cause DRD, and mutations in this gene should be considered in the differential diagnosis of unexplained DRD, particularly if the dystonia is cervical and if there is a recessive family history. ATM has previously been reported to cause isolated cervical dystonia, but never, to our knowledge, DRD. Individuals with dystonia related to ataxia telangiectasia may benefit from a trial of levodopa.
鉴定一个以常染色体隐性遗传方式遗传的穆斯林印度家族中,颈性多巴反应性肌张力障碍(DRD)的病因,此前该杂志曾对此进行过描述。
先前对导致 DRD 的基因(GCH1、TH 和 SPR)的突变检测均为阴性。对所有 3 名可提供 DNA 的受影响个体进行全外显子组测序,以鉴定潜在的致病性共享变异体。使用 OmniExpress 单核苷酸多态性芯片(Illumina,圣地亚哥,CA)对所有 3 名受影响个体获得的基因分型数据进行连锁分析、自交分析和拷贝数变异分析。使用 Sanger 测序对所有变体进行验证。
在对变体进行过滤后,外显子组测序显示 2 个基因含有潜在致病性的复合杂合变体(ATM 和 LRRC16A)。其中,ATM 中的变体与颈性 DRD 完全分离。已证实检测到的 ATM 中的两种突变均具有致病性,所有受影响个体的甲胎蛋白(一种共济失调毛细血管扩张症的标志物)均增加。
ATM 的双等位基因突变可导致 DRD,对于不明原因的 DRD,尤其是如果肌张力障碍是颈性的,并且有隐性家族史,应考虑该基因的突变。该基因以前曾被报道可引起孤立性颈性肌张力障碍,但据我们所知,从未引起过 DRD。与共济失调毛细血管扩张症相关的肌张力障碍患者可能受益于左旋多巴试验。