Please use this identifier to cite or link to this item: http://hdl.handle.net/2445/140516
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dc.contributor.authorCabré, Rosanna-
dc.contributor.authorNaudi, Alba-
dc.contributor.authorDomínguez González, Mayelín-
dc.contributor.authorAyala, Victòria-
dc.contributor.authorJove, Mariona-
dc.contributor.authorMota-Martorell, Natalia-
dc.contributor.authorPiñol Ripoll, Gerard-
dc.contributor.authorGil-Villar, Maria Pilar-
dc.contributor.authorRué, Montserrat-
dc.contributor.authorPortero Otin, Manuel-
dc.contributor.authorFerrer, Isidro (Ferrer Abizanda)-
dc.contributor.authorPamplona, Reinald-
dc.date.accessioned2019-09-19T14:46:32Z-
dc.date.available2019-09-19T14:46:32Z-
dc.date.issued2017-02-01-
dc.identifier.issn0891-5849-
dc.identifier.urihttp://hdl.handle.net/2445/140516-
dc.description.abstractHuman brain aging is the physiological process which underlies as cause of cognitive decline in the elderly and the main risk factor for neurodegenerative diseases such as Alzheimer's disease. Human neurons are functional throughout a healthy adult lifespan, yet the mechanisms that maintain function and protect against neurodegenerative processes during aging are unknown. Here we show that protein oxidative and glycoxidative damage significantly increases during human brain aging, with a breakpoint at 60 years old. This trajectory is coincident with a decrease in the content of the mitochondrial respiratory chain complex I to IV. We suggest that the deterioration in oxidative stress homeostasis during aging induces an adaptive response of stress resistance mechanisms based on the sustained expression of REST, and increased or decreased expression of Akt and mTOR, respectively, over the adult lifespan in order to preserve cell neural survival and function.-
dc.format.extent9 p.-
dc.format.mimetypeapplication/pdf-
dc.language.isoeng-
dc.publisherElsevier B.V.-
dc.relation.isformatofVersió postprint del document publicat a: https://doi.org/10.1016/j.freeradbiomed.2016.12.010-
dc.relation.ispartofFree Radical Biology and Medicine, 2017, vol. 103, p. 14-22-
dc.relation.urihttps://doi.org/10.1016/j.freeradbiomed.2016.12.010-
dc.rightscc-by-nc-nd (c) Elsevier B.V., 2017-
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/es-
dc.subject.classificationEnvelliment-
dc.subject.classificationLòbul frontal-
dc.subject.classificationMetabolisme-
dc.subject.otherAging-
dc.subject.otherFrontal lobe-
dc.subject.otherMetabolism-
dc.titleSixty years old is the breakpoint of human frontal cortex aging-
dc.typeinfo:eu-repo/semantics/article-
dc.typeinfo:eu-repo/semantics/acceptedVersion-
dc.identifier.idgrec690147-
dc.date.updated2019-09-19T14:46:32Z-
dc.rights.accessRightsinfo:eu-repo/semantics/openAccess-
Appears in Collections:Articles publicats en revistes (Patologia i Terapèutica Experimental)
Articles publicats en revistes (Institut de Recerca Biomèdica (IRB Barcelona))

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