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伴皮质下脑白质营养不良的震颤-共济失调(TACH)性脑白质营养不良定位于 10q22.3-10q23.31。

Tremor-ataxia with central hypomyelination (TACH) leukodystrophy maps to chromosome 10q22.3-10q23.31.

机构信息

Laboratoire de neurogénétique de la motricité, Neuromics Center for Excellence of Université de Montréal, CRCHUM, 1560 Sherbrooke East, Montreal, Quebec, H2L 4M1, Canada.

出版信息

Neurogenetics. 2010 Oct;11(4):457-64. doi: 10.1007/s10048-010-0251-8. Epub 2010 Jul 17.

Abstract

Leukodystrophies are a heterogeneous group of disorders associated with abnormal central nervous system white matter. The clinical features invariably include upper motor neuron signs and developmental regression with or without other neurological manifestations. The objective of this study was to characterize clinically and genetically a new form of childhood-onset leukodystrophy with ataxia and tremor. We recruited seven French-Canadian cases belonging to five families affected by an unknown form of childhood-onset leukodystrophy. Genome-wide scans (GWS) were performed using the Illumina Hap310 or Hap610 Bead Chip to identify regions of shared homozygosity that were further studied for linkage with STS markers. All cases presented between the ages of 1 and 5 years with spasticity along with other upper motor neuron signs, prominent postural tremor, and cerebellar signs. Though motor regression is a constant feature, cognitive functions are relatively preserved, even late in the course of the disease. The higher frequency of founder diseases in the French-Canadian population and the segregation in pedigrees are suggestive of a recessive mode of inheritance. By homozygosity mapping, we established linkage to a 12.6-Mb SNP-haplotyped region on chromosome 10q22.3-10q23.31 (maximum LOD score: 5.47). We describe an autosomal recessive childhood-onset leukodystrophy with ataxia and tremor mapping to a 12.6 Mb interval on chromosome 10q22.3-10q23.31. Identification of the mutated gene will allow precise diagnosis and genetic counseling and shed light on how its perturbed function leads to white matter abnormalities.

摘要

脑白质营养不良是一组与中枢神经系统白质异常相关的异质性疾病。其临床特征无一例外地包括上运动神经元体征和发育性倒退,伴有或不伴有其他神经表现。本研究的目的是对一种新的儿童起病的伴有共济失调和震颤的脑白质营养不良进行临床和基因特征分析。我们招募了 7 名来自 5 个家系的法裔加拿大患者,他们均患有一种不明原因的儿童起病的脑白质营养不良。使用 Illumina Hap310 或 Hap610 Bead Chip 进行全基因组扫描(GWS),以鉴定共享纯合性的区域,然后进一步使用 STS 标记物进行连锁分析。所有患者在 1 至 5 岁之间发病,表现为痉挛,伴有其他上运动神经元体征、明显姿势性震颤和小脑体征。尽管运动功能进行性倒退是一个常见特征,但认知功能相对保留,甚至在疾病晚期也是如此。法裔加拿大人群中高发的创始人疾病以及家系中的分离现象提示为隐性遗传模式。通过纯合性作图,我们确定了与 10q22.3-10q23.31 染色体上的 12.6Mb SNP 单体型区域的连锁关系(最大 LOD 评分:5.47)。我们描述了一种常染色体隐性遗传的儿童起病的伴有共济失调和震颤的脑白质营养不良,定位于 10q22.3-10q23.31 染色体上的 12.6Mb 区间。鉴定突变基因将能够进行精确的诊断和遗传咨询,并阐明其功能障碍如何导致白质异常。

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