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.

It is well known that mitochondria' 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.

Carri', M.t., Valle, C., Bozzo, F., Cozzolino, M. (2015). Oxidative stress and mitochondrial damage: Importance in non-SOD1 ALS. FRONTIERS IN CELLULAR NEUROSCIENCE, 9(FEB), 41 [10.3389/fncel.2015.00041].

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

CARRI', MARIA TERESA;
2015-01-01

Abstract

It is well known that mitochondria' 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.
2015
Pubblicato
Rilevanza internazionale
Articolo
Esperti anonimi
Settore BIO/10 - BIOCHIMICA
English
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.
ALS; Amyotrophic Lateral Sclerosis; mitochondria; neurodegeneration; oxidative stress
Carri', M.t., Valle, C., Bozzo, F., Cozzolino, M. (2015). Oxidative stress and mitochondrial damage: Importance in non-SOD1 ALS. FRONTIERS IN CELLULAR NEUROSCIENCE, 9(FEB), 41 [10.3389/fncel.2015.00041].
Carri', Mt; Valle, C; Bozzo, F; Cozzolino, M
Articolo su rivista
File in questo prodotto:
File Dimensione Formato  
FrontCellNeuro2015b.pdf

accesso aperto

Licenza: Non specificato
Dimensione 576.64 kB
Formato Adobe PDF
576.64 kB Adobe PDF Visualizza/Apri

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2108/123816
Citazioni
  • ???jsp.display-item.citation.pmc??? 45
  • Scopus 107
  • ???jsp.display-item.citation.isi??? 105
social impact