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

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.

Publication types

  • Case Reports

MeSH terms

  • Aged, 80 and over
  • Female
  • Humans
  • Male
  • Middle Aged
  • Motor Neuron Disease / enzymology*
  • Motor Neuron Disease / genetics*
  • Motor Neuron Disease / pathology
  • Motor Neuron Disease / physiopathology
  • Mutation*
  • Pedigree
  • Penetrance*
  • Superoxide Dismutase / genetics*
  • Superoxide Dismutase-1

Substances

  • SOD1 protein, human
  • Superoxide Dismutase
  • Superoxide Dismutase-1