Human Cu/Zn Superoxide Dismutase (SOD1) Overexpression in Mice Causes Mitochondrial Vacuolization, Axonal Degeneration, and Premature Motoneuron Death and Accelerates Motoneuron Disease in Mice Expressing a Familial Amyotrophic Lateral Sclerosis Mutant SOD1

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Cited by papers we hold 7

• Alterations in lipid metabolism of spinal cord linked to amyotrophic lateral sclerosis · 2019
  No notice
• Bee Venom: Overview of Main Compounds and Bioactivities for Therapeutic Interests · 2019
  No notice
• Targeting Nrf2 to Suppress Ferroptosis and Mitochondrial Dysfunction in Neurodegeneration · 2018
  No notice
• Energy metabolism in ALS: an underappreciated opportunity? · 2018
  No notice
• Characterization of early pathogenesis in the SOD 1 G93A mouse model of ALS : part II, results and discussion · 2013
  No notice
• Novel Antibodies Reveal Inclusions Containing Non-Native SOD1 in Sporadic ALS Patients · 2010
  No notice
• Protein Aggregation and Protein Instability Govern Familial Amyotrophic Lateral Sclerosis Patient Survival · 2008
  No notice

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