Evolution of gait abnormalities in SOD1 G93A transgenic mice

Renzo Mancuso, Sara Oliván, Rosario Osta, Xavier Navarro

Research output: Contribution to journalArticleResearchpeer-review

43 Citations (Scopus)

Abstract

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder characterized by the loss of upper and lower motoneurons. Clinically, it is manifested by weakness, muscle atrophy and progressive paralysis and ends up with patients' death 2-5 years after diagnosis. Although these symptoms lead in many cases to gait deficits in patients, an exhaustive locomotor profile of animal models mimicking the disease has not been assessed yet. In this work we evaluated the locomotor performance of the SOD1 G93A mouse model of ALS using computerized treadmill gait analysis. SOD1 G93A mice presented early (8 weeks of age) gait abnormalities, evidenced by an increase in the time of the propulsion phase of hindlimb stance. The alterations progressed during the disease until a complete disturbance of normal gait. This finding is meaningful to the field because the identification of a significant difference in a functional endpoint as early as 8 weeks might be a step forward resolving the debate about treatment of mice prior to the symptomatic phase in efficacy studies. These results also point out that digitizing analysis of treadmill locomotion may be useful to evaluate whether new therapeutic approaches are improving functional outcome of the animals. © 2011 Elsevier B.V. All rights reserved.
Original languageEnglish
Pages (from-to)65-73
JournalBrain Research
Volume1406
DOIs
Publication statusPublished - 11 Aug 2011

Keywords

  • Locomotion
  • Motoneuron disease
  • Neurodegeneration
  • SOD1 mouse

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