ArticleBiochimica et biophysica acta
Presymptomatic biochemical changes in hindlimb muscle of G93A human Cu/Zn superoxide dismutase 1 transgenic mouse model of amyotrophic lateral sclerosis.
Article in Biochimica et biophysica acta. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 21 citations in OpenAlex.
- New perspectives of the role of skeletal muscle derived extracellular vesicles in the pathogenesis of amyotrophic lateral sclerosis: the 'dying back' hypothesis.Journal of extracellular biology · 2024Review
- ALS Skeletal Muscle: Victim or Culprit.The neuroscience chronicles · 2021Article
- Neuromuscular Development and Disease: Learning FromFrontiers in cell and developmental biology · 2021Review
- Running and swimming prevent the deregulation of the BDNF/TrkB neurotrophic signalling at the neuromuscular junction in mice with amyotrophic lateral sclerosis.Cellular and molecular life sciences : CMLS · 2020Article
- The Role of Skeletal Muscle in Amyotrophic Lateral Sclerosis.Brain pathology (Zurich, Switzerland) · 2016Review
- CD4 + T Cells and Neuroprotection: Relevance to Motoneuron Injury and Disease.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2015Review
- Defective mitochondrial dynamics is an early event in skeletal muscle of an amyotrophic lateral sclerosis mouse model.PloS one · 2013Article
- Postnatal muscle modification by myogenic factors modulates neuropathology and survival in an ALS mouse model.Nature communications · 2013Article
- The anabolic/androgenic steroid nandrolone exacerbates gene expression modifications induced by mutant SOD1 in muscles of mice models of amyotrophic lateral sclerosis.Pharmacological research · 2012Article
- Administration of Recombinant Heat Shock Protein 70 Delays Peripheral Muscle Denervation in the SOD1(G93A) Mouse Model of Amyotrophic Lateral Sclerosis.Neurology research international · 2012Article
- Differential gene expression in the axotomized facial motor nucleus of presymptomatic SOD1 mice.The Journal of comparative neurology · 2011Article
- Stronger is not always better: could a bodybuilding dietary supplement lead to ALS?Experimental neurology · 2011Review
- The "dying-back" phenomenon of motor neurons in ALS.Journal of molecular neuroscience : MN · 2011Review
- Hyperactive intracellular calcium signaling associated with localized mitochondrial defects in skeletal muscle of an animal model of amyotrophic lateral sclerosis.The Journal of biological chemistry · 2010Article
- Mitochondrial dysfunction in amyotrophic lateral sclerosis.Biochimica et biophysica acta · 2010Review
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2 authors at 1 institution in 1 country.
Funding
Abstract
Amyotrophic lateral sclerosis (ALS) is primarily a motor neuron disorder. Intriguingly, early muscle denervation preceding motor neuron loss is observed in mouse models of ALS. Enhanced muscle vulnerability to denervation process has been suggested by accelerated muscle deterioration following peripheral nerve injury in an ALS mouse model. Here we provide evidence of biochemical changes in the hindlimb muscle of young, presymptomatic G93A hSOD1 transgenic mice. In this report, we demonstrate that cdk5 activity is reduced in hindlimb muscle of 27-day-old G93A hSOD1 transgenic mice. In vitro analysis revealed mutant hSOD1-mediated suppression of cdk5 activity. Furthermore, the decrease in muscle cdk5 activity was accompanied by a significant reduction in MyoD and cyclin D1 levels. These early muscle changes raise the possibility that the progressive deterioration of muscle function is potentiated by altered muscle biochemistry in these mice at a very young, presymptomatic age.
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