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一种新的 KIF5A 基因突变导致遗传性痉挛性截瘫伴轴索性神经病。

A novel mutation in KIF5A gene causing hereditary spastic paraplegia with axonal neuropathy.

机构信息

Department of Neurosciences, Psychiatry and Anaesthesiology, University of Messina, Messina, Italy.

出版信息

Neurol Sci. 2011 Aug;32(4):665-8. doi: 10.1007/s10072-010-0445-8. Epub 2010 Nov 24.

Abstract

Hereditary spastic paraplegias (HSPs) include a group of neurodegenerative diseases, and so far 46 SPG loci have been mapped and 17 genes isolated. Among the autosomal dominant HSPs (AD-HSPs), SPG10 is a rare form due to mutations in KIF5A gene (locus 12q13.3). We describe the clinical, neurophysiological, morphological and genetic study of an Italian family with AD-HSP. The proband presented with an adult onset spastic paraparesis and diffuse paresthesias where neurophysiological and nerve biopsy morphological studies revealed an axonal neuropathy. Molecular genetic analysis identified a new missense mutation (c.608C>G) of KIF5A gene resulting in a serine to cysteine substitution, S203C, located in a highly conserved domain of the protein. This pedigree confirms the occurrence of an axonal peripheral neuropathy in SPG10.

摘要

遗传性痉挛性截瘫(HSP)包括一组神经退行性疾病,迄今为止已经定位了 46 个 SPG 基因座并分离出了 17 个基因。在常染色体显性遗传性痉挛性截瘫(AD-HSP)中,由于 KIF5A 基因突变(位于 12q13.3 号染色体),SPG10 是一种罕见形式。我们描述了一个意大利 AD-HSP 家族的临床、神经生理学、形态学和遗传学研究。先证者表现为成年起病的痉挛性截瘫和弥漫性感觉异常,神经生理学和神经活检形态学研究显示为轴索性神经病。分子遗传学分析发现 KIF5A 基因的一个新错义突变(c.608C>G),导致丝氨酸到半胱氨酸取代,即 S203C,位于该蛋白高度保守的结构域中。该家系证实了 SPG10 存在轴索性周围神经病。

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