English   español  
Please use this identifier to cite or link to this item: http://hdl.handle.net/10261/77536
Share/Impact:
Statistics
logo share SHARE logo core CORE   Add this article to your Mendeley library MendeleyBASE

Visualizar otros formatos: MARC | Dublin Core | RDF | ORE | MODS | METS | DIDL
Exportar a otros formatos:

Title

Oxidative stress and altered mitochondrial function in neurodegenerative diseases: lessons from mouse models

AuthorsFernández-Checa, José C. ; Fernández, Anna; Morales, Albert ; Marí, Montserrat ; García-Ruiz, Carmen ; Colell Riera, Anna
Issue Date2010
PublisherBentham Science Publishers
CitationCNS and Neurological Disorders - Drug Targets 9(4): 439-454 (2010)
AbstractOxidative stress has been consistently linked to ageing-related neurodegenerative diseases leading to the generation of lipid peroxides, carbonyl proteins and oxidative DNA damage in tissue samples from affected brains. Studies from mouse models that express disease-specific mutant proteins associated to the major neurodegenerative processes have underscored a critical role of mitochondria in the pathogenesis of these diseases. There is strong evidence that mitochondrial dysfunction is an early event in neurodegeneration. Mitochondria are the main cellular source of reactive oxygen species and key regulators of cell death. Moreover, mitochondria are highly dynamic organelles that divide, fuse and move along axons and dendrites to supply cellular energetic demands; therefore, impairment of any of these processes would directly impact on neuronal viability. Most of the disease-specific pathogenic mutant proteins have been shown to target mitochondria, promoting oxidative stress and the mitochondrial apoptotic pathway. In addition, disease-specific mutant proteins may also impair mitochondrial dynamics and recycling of damaged mitochondria via autophagy. Collectively, these data suggest that ROS-mediated defective mitochondria may accumulate during and contribute to disease progression. Strategies aimed to improve mitochondrial function or ROS scavenging may thus be of potential clinical relevance. © 2010 Bentham Science Publishers Ltd.
DescriptionEl pdf del artículo es la versión post-print.
Publisher version (URL)http://dx.doi.org/10.2174/187152710791556113
URIhttp://hdl.handle.net/10261/77536
DOI10.2174/187152710791556113
Identifiersdoi: 10.2174/187152710791556113
issn: 1871-5273
e-issn: 1996-3181
Appears in Collections:(IIBB) Artículos
Files in This Item:
File Description SizeFormat 
Oxidative stress and altered.pdfArtículo256,12 kBAdobe PDFThumbnail
View/Open
FIGURAS CNSND_Fernandez-Checa et al.pdfFiguras756,41 kBAdobe PDFThumbnail
View/Open
Show full item record
Review this work
 

Related articles:


WARNING: Items in Digital.CSIC are protected by copyright, with all rights reserved, unless otherwise indicated.