van Swieten John C, Brusse Esther, de Graaf Bianca M, Krieger Elmar, van de Graaf Raoul, de Koning Inge, Maat-Kievit Anneke, Leegwater Peter, Dooijes Dennis, Oostra Ben A, Heutink Peter
Department of Neurology, Erasmus Medical Center, Rotterdam, The Netherlands.
Am J Hum Genet. 2003 Jan;72(1):191-9. doi: 10.1086/345488. Epub 2002 Dec 13.
Hereditary spinocerebellar ataxias (SCAs) are a clinically and genetically heterogeneous group of neurodegenerative disorders for which >/=14 different genetic loci have been identified. In some SCA types, expanded tri- or pentanucleotide repeats have been identified, and the length of these expansions correlates with the age at onset and with the severity of the clinical phenotype. In several other SCA types, no genetic defect has yet been identified. We describe a large, three-generation family with early-onset tremor, dyskinesia, and slowly progressive cerebellar ataxia, not associated with any of the known SCA loci, and a mutation in the fibroblast growth factor 14 (FGF14) gene on chromosome 13q34. Our observations are in accordance with the occurrence of ataxia and paroxysmal dyskinesia in Fgf14-knockout mice. As indicated by protein modeling, the amino acid change from phenylalanine to serine at position 145 is predicted to reduce the stability of the protein. The present FGF14 mutation represents a novel gene defect involved in the neurodegeneration of cerebellum and basal ganglia.
遗传性脊髓小脑共济失调(SCAs)是一组临床和遗传异质性的神经退行性疾病,已确定了≥14个不同的基因位点。在某些SCA类型中,已发现三核苷酸或五核苷酸重复序列扩增,这些扩增的长度与发病年龄和临床表型的严重程度相关。在其他几种SCA类型中,尚未发现基因缺陷。我们描述了一个三代大家庭,其成员患有早发性震颤、运动障碍和缓慢进展的小脑共济失调,与任何已知的SCA基因位点均无关联,并且在13q34染色体上的成纤维细胞生长因子14(FGF14)基因中发现了一个突变。我们的观察结果与Fgf14基因敲除小鼠中出现共济失调和阵发性运动障碍一致。蛋白质建模表明,第145位氨基酸从苯丙氨酸变为丝氨酸预计会降低蛋白质的稳定性。目前的FGF14突变代表了一种与小脑和基底神经节神经退行性变有关的新的基因缺陷。