Oxidative Stress and Mitochondrial Damage: Importance in Non-SOD1 ALS

Overview

Journal Front Cell Neurosci

Specialty Cell Biology

Date 2015 Mar 6

PMID 25741238

Citations 59

Authors

Maria Teresa Carri

Cristiana Valle

Francesca Bozzo

Mauro Cozzolino

Affiliations

Soon will be listed here.

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.

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