A mouse model of familial ALS has increased CNS levels of endogenous ubiquinol9/10 and does not benefit from exogenous administration of ubiquinol10.

A mouse model of familial ALS has increased CNS levels of endogenous ubiquinol9/10 and does not benefit from exogenous administration of ubiquinol10.

Oxidative stress and mitochondrial impairment are the main pathogenic mechanisms of Amyotrophic Lateral Sclerosis (ALS), a severe neurodegenerative disease still lacking of effective therapy. Recently, the coenzyme-Q (CoQ) complex, a key component of mitochondrial function and redox-state modulator,...

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Main Authors: Jacopo Lucchetti, Marianna Marino, Simonetta Papa, Massimo Tortarolo, Giovanna Guiso, Silvia Pozzi, Valentina Bonetto, Silvio Caccia, Ettore Beghi, Caterina Bendotti, Marco Gobbi
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2013-01-01
Series:PLoS ONE
Online Access:https://doi.org/10.1371/journal.pone.0069540
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https://doi.org/10.1371/journal.pone.0069540

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