Neurodegeneration in amyotrophic lateral sclerosis : the role of oxidative stress and altered homeostasis of metals (Articolo in rivista)

Type

• Prodotto della ricerca (Classe)
• Articolo in rivista (Classe)

Label

• Neurodegeneration in amyotrophic lateral sclerosis : the role of oxidative stress and altered homeostasis of metals (Articolo in rivista) (literal)

Anno

• 2003-01-01T00:00:00+01:00 (literal)

Alternative label

• Carrì M.T., Ferri A., Cozzolino M., Calabrese L. and Rotilio G (2003)
  Neurodegeneration in amyotrophic lateral sclerosis : the role of oxidative stress and altered homeostasis of metals
  in Brain research bulletin
  (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori

• Carrì M.T., Ferri A., Cozzolino M., Calabrese L. and Rotilio G (literal)

Pagina inizio

• 365 (literal)

Pagina fine

• 374 (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume

• 61 (literal)

Rivista

• Brain research bulletin (Rivista)

Note

• ISI Web of Science (WOS) (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni

• Istituto di Biologia Cellulare e Neurobiologia (literal)

Titolo

• Neurodegeneration in amyotrophic lateral sclerosis : the role of oxidative stress and altered homeostasis of metals (literal)

Abstract

• Amyotrophic lateral sclerosis is one of the most common neurodegenerative disorders, with an incidence of about 1/100,000. One of the typical features of this progressive, lethal disease, occurring both sporadically and as a familial disorder, is degeneration of cortical and spinal motor neurones. Present evidence indicates that loss of neurones in patients results from a complex interplay among oxidative injury, excitotoxic stimulation, dysfunction of critical proteins and genetic factors. This review focuses on existing evidence that oxidative stress is a major culprit in the pathogenesis of amyotrophic lateral sclerosis. An increase in reactive oxygen species and in products of oxidation has been observed both in post-mortem samples and in experimental models for ALS. This increase may be consequent to altered metabolism of copper and iron ions, that share the property to undergo redox cycling and generate reactive oxygen species. Metal-mediated oxidative stress would lead to several intracellular alterations and contribute to the induction of cell death pathways. (literal)

Prodotto di

• Institute of neuroscience (IN) (Istituto)
• ex SV.P16.003.002 / Studio dei meccanismi molecolari di processi neurodegenerativi (SV.P16.003.005) (Modulo)

Autore CNR

• ALBERTO FERRI (Unità di personale interno)

Incoming links:

Autore CNR di

• ALBERTO FERRI (Unità di personale interno)

Prodotto

• Institute of neuroscience (IN) (Istituto)
• ex SV.P16.003.002 / Studio dei meccanismi molecolari di processi neurodegenerativi (SV.P16.003.005) (Modulo)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#rivistaDi

• Brain research bulletin (Rivista)