Elter Tim Lukas, Sturm Daniel, Santana Magda M, Schaprian Tamara, Raposo Mafalda, Melo Ana Rosa Vieira, Lima Manuela, Koyak Berkan, Oender Demet, Grobe-Einsler Marcus, Lopes Sara, Silva Patrick, de Almeida Luís Pereira, Giunti Paola, Garcia-Moreno Hector, Nethisinhe Suran, de Vries Jeroen, van de Warrenburg Bart P, van Gaalen Judith, Synofzik Matthis, Schöls Ludger, Reetz Kathrin, Erdlenbruch Friedrich, Jacobi Heike, Infante Jon, Riess Olaf, Klockgether Thomas, Faber Jennifer, Hübener-Schmid Jeannette
German Center for Neurodegenerative Diseases, Clinical Research, Venusberg-Campus 1/99, 53127, Bonn, Germany.
Institute for Medical Genetics and Applied Genomics, University of Tuebingen, Tuebingen, Germany.
J Neurol. 2024 Dec 12;272(1):54. doi: 10.1007/s00415-024-12829-9.
Knowledge about the distribution and frequency of the respective haplotypes on the wildtype and mutant allele is highly relevant in the context of future gene therapy clinical studies in Spinocerebellar Ataxia Type 3, the most common autosomal dominantly inherited ataxia. Single nucleotide polymorphisms associated to the disease-causing gene, ATXN3, have been determined. We wanted to investigate the frequency and regional distribution of two intragenic single nucleotide polymorphisms (SNPs) in a large European SCA3 cohort and their relation to the clinical phenotype.
The genotypes of the two polymorphisms at base pair positions 987 and 1118 of the ATXN3 were determined for their co-localization on the normal and expanded allele, respectively, in 286 SCA3 mutation carriers and 117 healthy controls from 11 European sites.
The distribution of genotypes on the expanded allele differed from those of the wildtype allele of SCA3 mutation carriers and of healthy controls, and was mainly influenced by the regional origin. In our cohort, no particular clinical phenotype was associated with any specific haplotype.
Our results confirm distinct allocations of SNPs associated to the expanded ATXN3, and accordingly the consideration of allele-specific therapies.
在未来针对最常见的常染色体显性遗传性共济失调——脊髓小脑共济失调3型(Spinocerebellar Ataxia Type 3)的基因治疗临床研究中,了解野生型和突变等位基因上各自单倍型的分布和频率具有高度相关性。已确定了与致病基因ATXN3相关的单核苷酸多态性。我们想要研究在一个大型欧洲脊髓小脑共济失调3型队列中两个基因内单核苷酸多态性(SNP)的频率和区域分布,以及它们与临床表型的关系。
在来自欧洲11个地点的286名脊髓小脑共济失调3型突变携带者和117名健康对照中,分别确定了ATXN3基因第987和1118个碱基对位置处两个多态性的基因型,以了解它们在正常和扩展等位基因上的共定位情况。
扩展等位基因上的基因型分布与脊髓小脑共济失调3型突变携带者的野生型等位基因以及健康对照的不同,并且主要受区域来源影响。在我们的队列中,没有任何特定临床表型与任何特定单倍型相关。
我们的结果证实了与扩展的ATXN3相关的单核苷酸多态性的不同分布,因此支持考虑等位基因特异性疗法。