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家族性新型超氧化物歧化酶1(SOD1)突变所致散发性运动神经元病:不完全外显还是偶然关联?

Sporadic motor neuron disease in a familial novel SOD1 mutation: incomplete penetrance or chance association?

作者信息

Conforti Francesca L, Barone Rita, Fermo Salvatore Lo, Giliberto Claudia, Patti Francesco, Gambardella Antonio, Quattrone Aldo, Zappia Mario

机构信息

Department of Neurosciences, University of Catania, Catania, Italy.

出版信息

Amyotroph Lateral Scler. 2011 May;12(3):220-2. doi: 10.3109/17482968.2010.545951.

Abstract

Cu/Zn superoxide dismutase (SOD1) gene mutations have been reported in familial and sporadic amyotrophic lateral sclerosis (ALS). We report a novel G61R SOD1 mutation in a patient with a distinct phenotype including prominent lower motor neuron dysfunction, proximal weakness and atrophy with asymmetrical onset in the thigh and buttock and relentless clinical course. The G61R mutation segregated in three unaffected relatives including the 80-year-old mother and two of the proband's siblings. Potential mechanisms include an autosomal dominant condition with reduced penetrance or a chance association.

摘要

家族性和散发性肌萎缩侧索硬化症(ALS)中均有铜/锌超氧化物歧化酶(SOD1)基因突变的报道。我们报告了1例具有独特表型的患者,其携带新型G61R SOD1突变,该表型包括明显的下运动神经元功能障碍、近端肌无力和萎缩,起病不对称,累及大腿和臀部,临床病程呈进行性。G61R突变在3名未受影响的亲属中分离,包括80岁的母亲和先证者的2名兄弟姐妹。潜在机制包括外显率降低的常染色体显性疾病或偶然关联。

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