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dc.contributor.authorSorolla Bardají, Maria Alba
dc.contributor.authorReverter Branchat, Gemma
dc.contributor.authorTamarit Sumalla, Jordi
dc.contributor.authorFerrer, Isidre
dc.contributor.authorRos Salvador, Joaquim
dc.contributor.authorCabiscol Català, Elisa
dc.date.accessioned2016-06-06T10:32:52Z
dc.date.issued2008
dc.identifier.issn0891-5849
dc.identifier.urihttp://hdl.handle.net/10459.1/57161
dc.description.abstractHuntington disease (HD) is a neurodegenerative disorder caused by expansion of CAG repeats in exon 1 of the huntingtin gene, affecting initially the striatum and progressively the cortex. This work reports a proteomic analysis of human brain postmortem samples obtained from striatum and cortex of patients with HD compared to samples of age- and sex-matched controls. Antioxidant defense proteins that were strongly induced in striatum, but also detectable in cortex, were identified as peroxiredoxins 1, 2, and 6, as well as glutathione peroxidases 1 and 6. The activities of other antioxidant enzymes such as mitochondrial superoxide dismutase and catalase were also increased in HD. Aconitase, a protein involved in energy metabolism, showed decreased activities in striatum of HD patients. Protein carbonyls, used as markers of oxidative stress, were increased in HD, and glial fibrillary acidic protein, aconitase, γ-enolase, and creatine kinase B were identified as the main targets. Taken together, these results indicate that oxidative stress and damage to specific macromolecules would participate in the disease progression. Also, these data support the rationale for therapeutic strategies that either potentiate antioxidant defenses or avoid oxidative stress generation to delay disease progression.ca_ES
dc.description.sponsorshipThis work has been supported by Grants BFU2004-00593/BMC, BFU2007-66249, and CSD2007-20 Consolider Ingenio 2010 from the Ministerio de Educación y Ciencia (Spain) and SGR2005-00677 from the Generalitat de Catalunya. M. A. Sorolla is the recipient of a Ph.D. fellowship from the Ministerio de Educación y Ciencia (Spain)ca_ES
dc.language.isoengca_ES
dc.publisherElsevierca_ES
dc.relationMIECI/PN2004-2007/BFU2004-00593/BMC
dc.relationMIECI/PN2004-2007/BFU2007-66249
dc.relation.isformatofReproducció del document publicat a https://doi.org/10.1016/j.freeradbiomed.2008.05.014ca_ES
dc.relation.ispartofFree Radical Biology and Medicine, 2008, vol. 45, núm. 5, p. 667-678ca_ES
dc.rights(c) Elsevier Inc., 2008ca_ES
dc.subjectHuntington diseaseca_ES
dc.subjectProteomic analysisca_ES
dc.subjectOxidative stressca_ES
dc.subjectProtein carbonylationca_ES
dc.titleProteomic and oxidative stress analysis in human brain samples of Huntington diseaseca_ES
dc.typearticleca_ES
dc.identifier.idgrec012451
dc.type.versionpublishedVersionca_ES
dc.rights.accessRightsinfo:eu-repo/semantics/restrictedAccessca_ES
dc.identifier.doihttps://doi.org/10.1016/j.freeradbiomed.2008.05.014
dc.date.embargoEndDate10000-01-01


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