Abstract
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'.
Original language | English |
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Pages (from-to) | 44-49 |
Number of pages | 6 |
Journal | Molecular and Cellular Neuroscience |
Volume | 55 |
DOIs | |
Publication status | Published - Jul 2013 |
Keywords
- Amyotrophic lateral sclerosis
- Mitochondria
- Oxidative stress
ASJC Scopus subject areas
- Molecular Biology
- Cellular and Molecular Neuroscience
- Cell Biology