Mitochondria and ALS: Implications from novel genes and pathways
Evidence from patients with sporadic and familiar amyotrophic lateral sclerosis (ALS) and from models based on the overexpression of mutant SOD1 found in a small subset of patients, clearly point to mitochondrial damage as a relevant facet of this neurodegenerative condition. In this mini-review we...
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Veröffentlicht in: | Molecular and cellular neuroscience 2013-07, Vol.55, p.44-49 |
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creator | Cozzolino, Mauro Ferri, Alberto Valle, Cristiana Carrì, Maria Teresa |
description | Evidence from patients with sporadic and familiar amyotrophic lateral sclerosis (ALS) and from models based on the overexpression of mutant SOD1 found in a small subset of patients, clearly point to mitochondrial damage as a relevant facet of this neurodegenerative condition. In this mini-review we provide a brief update on the subject in the light of newly discovered genes (such as TDP-43 and FUS/TLS) associated to familial ALS and of a deeper knowledge of the mechanisms of derangement of mitochondria. This article is part of a Special Issue entitled 'Mitochondrial function and dysfunction in neurodegeneration'. |
doi_str_mv | 10.1016/j.mcn.2012.06.001 |
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subjects | Amyotrophic lateral sclerosis Amyotrophic Lateral Sclerosis - genetics Amyotrophic Lateral Sclerosis - metabolism Animals DNA-Binding Proteins - genetics DNA-Binding Proteins - metabolism Genes, Mitochondrial Humans Mitochondria Mitochondria - genetics Mitochondria - metabolism Oxidative stress RNA-Binding Protein FUS - genetics RNA-Binding Protein FUS - metabolism |
title | Mitochondria and ALS: Implications from novel genes and pathways |
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