Oxidative stress and mitochondrial damage: Importance in non-SOD1 ALS

Maria Teresa Carrì, Cristiana Valle, Francesca Bozzo, Mauro Cozzolino

Research output: Contribution to journalArticlepeer-review

Abstract

It is well known that mitochondrial damage (MD) is both the major contributor to oxidative stress (OS) (the condition arising from unbalance between production and removal of reactive oxygen species) and one of the major consequences of OS, because of the high dependance of mitochondrial function on redox-sensitive targets such as intact membranes. Conditions in which neuronal cells are not able to cope with MD and OS seem to lead or contribute to several neurodegenerative diseases including Amyotrophic Lateral Sclerosis (ALS), at least in the most studied superoxide dismutase 1 (SOD1)-linked genetic variant. As summarized in this review, new evidence indicates that MD and OS play a role also in non-SOD1 ALS and thus they may represent a target for therapy despite previous failures in clinical trials.

Original languageEnglish
JournalFrontiers in Cellular Neuroscience
Volume9
Issue numberFEB
DOIs
Publication statusPublished - Feb 17 2015

Keywords

  • ALS
  • Amyotrophic lateral sclerosis
  • Mitochondria
  • Neurodegeneration
  • Oxidative stress

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience

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