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

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...

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Bibliographic Details
Published in:Frontiers in cellular neuroscience 2015-02, Vol.9, p.41-41
Main Authors: Carrì, Maria Teresa, Valle, Cristiana, Bozzo, Francesca, Cozzolino, Mauro
Format: Article
Language:English
Subjects:
ALS
Amyotrophic Lateral Sclerosis
Apoptosis
Clinical trials
Genetic diversity
Insects
Localization
Mitochondria
Motor neurone disease
Mutation
Neurodegeneration
Neurodegenerative diseases
Neuroscience
Neurosciences
Oxidative Stress
Pathogenesis
Pathology
Proteins
Reactive oxygen species
Superoxide dismutase
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Summary: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.
ISSN:1662-5102
1662-5102
DOI:10.3389/fncel.2015.00041