Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8478694 | Molecular and Cellular Neuroscience | 2013 | 6 Pages |
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'.
Keywords
Cu, Zn superoxide dismutasefused in sarcoma/translocated in liposarcomaTAR DNA binding protein 43GSHHDACCFPVAPBTDP-43SOD1UPRFUS/TLSROSamyotrophic lateral sclerosisALSOxidative stressendoplasmic reticulumMitochondriahistone acetyl transferasehistone deacetylaseUnfolded protein responsecyan fluorescent proteinHATGlutathione
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Authors
Mauro Cozzolino, Alberto Ferri, Cristiana Valle, Maria Teresa Carrì,