Erythropoietin delays disease onset in an amyotrophic lateral sclerosis model

Exp Neurol. 2007 Mar;204(1):260-3. doi: 10.1016/j.expneurol.2006.11.002. Epub 2006 Dec 15.

Abstract

Erythropoietin (Epo) has been shown in the recent years to have neuroprotective activity in a variety of settings. In this study, we investigated its impact on the progression of paralysis in a mouse model simulating the human disorder amyotrophic lateral sclerosis (ALS). We found that Epo can delay the onset of motor deterioration in transgenic SOD G93A mice without prolonging their survival. Notably this effect was selective for the females only. These initial findings encourage further investigation of this biological avenue in the search for improved remedies for this fatal disease.

MeSH terms

  • Adenine
  • Amyotrophic Lateral Sclerosis / genetics
  • Amyotrophic Lateral Sclerosis / pathology
  • Amyotrophic Lateral Sclerosis / physiopathology*
  • Amyotrophic Lateral Sclerosis / prevention & control*
  • Animals
  • Disease Progression
  • Erythropoietin / administration & dosage
  • Erythropoietin / pharmacology*
  • Female
  • Guanine
  • Humans
  • Injections, Intraperitoneal
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Motor Activity / drug effects
  • Motor Neurons / pathology
  • Mutation
  • Neuroprotective Agents / administration & dosage
  • Neuroprotective Agents / pharmacology*
  • Recombinant Proteins
  • Sex Factors
  • Spinal Cord / pathology
  • Superoxide Dismutase / genetics
  • Superoxide Dismutase-1
  • Time Factors

Substances

  • Neuroprotective Agents
  • Recombinant Proteins
  • SOD1 protein, human
  • Erythropoietin
  • Guanine
  • Sod1 protein, mouse
  • Superoxide Dismutase
  • Superoxide Dismutase-1
  • Adenine