Mechanisms of muscle denervation in aging: Insights from a Mouse Model of Amyotrophic Lateral Sclerosis

Research output: Contribution to journalReview articlepeer-review

21 Scopus citations

Abstract

Muscle denervation at the neuromuscular junction (NMJ) is thought to be a contributing factor in age-related muscle weakness. Therefore, understanding the mechanisms that modulate NMJ innervation is a key to developing therapies to combat age-related muscle weakness affecting the elderly. Two mouse models, one lacking the Cu/Zn superoxide dismutase (SOD1) gene and another harboring the transgenic mutant human SOD1 gene, display progressive changes at the NMJ, including muscle endplate fragmentation, nerve terminal sprouting, and denervation. These changes at the NMJ share many of the common features observed in the NMJs of aged mice. In this review, research findings demonstrating the effects of PGC-1a, IGF-1, GDNF, MyoD, myogenin, and miR-206 on NMJ innervation patterns in the G93A SOD1 mice will be highlighted in the context of age-related muscle denervation.

Original languageEnglish
Pages (from-to)380-389
Number of pages10
JournalAging and Disease
Volume6
Issue number5
DOIs
StatePublished - 2015

Keywords

  • Aging
  • Amyotrophic lateral sclerosis
  • G93A SOD1 mouse
  • Muscle denervation
  • Oxidative stress
  • SOD1 mouse

Fingerprint

Dive into the research topics of 'Mechanisms of muscle denervation in aging: Insights from a Mouse Model of Amyotrophic Lateral Sclerosis'. Together they form a unique fingerprint.

Cite this