Sixty years old is the breakpoint of human frontal cortex aging

Human 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 fun...

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Detalles Bibliográficos
Autores: Cabré, Rosanna, Naudi, Alba, Domínguez González, Mayelín, Ayala, Victòria, Jove, Mariona, Mota-Martorell, Natalia, Piñol Ripoll, Gerard, Gil-Villar, Maria Pilar, Rué, Montserrat, Portero-Otin, Manuel, Ferrer, Isidro (Ferrer Abizanda), Pamplona, Reinald
Tipo de recurso: artículo
Estado:Versión aceptada para publicación
Fecha de publicación:2017
País:España
Institución:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
Repositorio:Recercat. Dipósit de la Recerca de Catalunya
OAI Identifier:oai:recercat.cat:2445/140516
Acceso en línea:https://hdl.handle.net/2445/140516
Access Level:acceso abierto
Palabra clave:Envelliment
Lòbul frontal
Metabolisme
Aging
Frontal lobe
Metabolism
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spelling Sixty years old is the breakpoint of human frontal cortex agingCabré, RosannaNaudi, AlbaDomínguez González, MayelínAyala, VictòriaJove, MarionaMota-Martorell, NataliaPiñol Ripoll, GerardGil-Villar, Maria PilarRué, MontserratPortero-Otin, ManuelFerrer, Isidro (Ferrer Abizanda)Pamplona, ReinaldEnvellimentLòbul frontalMetabolismeAgingFrontal lobeMetabolismHuman 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.Elsevier B.V.2019201920172019info:eu-repo/semantics/articleinfo:eu-repo/semantics/acceptedVersion9 p.application/pdfhttps://hdl.handle.net/2445/140516Articles publicats en revistes (Patologia i Terapèutica Experimental)reponame:Recercat. Dipósit de la Recerca de Catalunyainstname:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)InglésVersió postprint del document publicat a: https://doi.org/10.1016/j.freeradbiomed.2016.12.010Free Radical Biology and Medicine, 2017, vol. 103, p. 14-22https://doi.org/10.1016/j.freeradbiomed.2016.12.010cc-by-nc-nd (c) Elsevier B.V., 2017http://creativecommons.org/licenses/by-nc-nd/3.0/esinfo:eu-repo/semantics/openAccessoai:recercat.cat:2445/1405162026-05-29T05:05:01Z
dc.title.none.fl_str_mv Sixty years old is the breakpoint of human frontal cortex aging
title Sixty years old is the breakpoint of human frontal cortex aging
spellingShingle Sixty years old is the breakpoint of human frontal cortex aging
Cabré, Rosanna
Envelliment
Lòbul frontal
Metabolisme
Aging
Frontal lobe
Metabolism
title_short Sixty years old is the breakpoint of human frontal cortex aging
title_full Sixty years old is the breakpoint of human frontal cortex aging
title_fullStr Sixty years old is the breakpoint of human frontal cortex aging
title_full_unstemmed Sixty years old is the breakpoint of human frontal cortex aging
title_sort Sixty years old is the breakpoint of human frontal cortex aging
dc.creator.none.fl_str_mv Cabré, Rosanna
Naudi, Alba
Domínguez González, Mayelín
Ayala, Victòria
Jove, Mariona
Mota-Martorell, Natalia
Piñol Ripoll, Gerard
Gil-Villar, Maria Pilar
Rué, Montserrat
Portero-Otin, Manuel
Ferrer, Isidro (Ferrer Abizanda)
Pamplona, Reinald
author Cabré, Rosanna
author_facet Cabré, Rosanna
Naudi, Alba
Domínguez González, Mayelín
Ayala, Victòria
Jove, Mariona
Mota-Martorell, Natalia
Piñol Ripoll, Gerard
Gil-Villar, Maria Pilar
Rué, Montserrat
Portero-Otin, Manuel
Ferrer, Isidro (Ferrer Abizanda)
Pamplona, Reinald
author_role author
author2 Naudi, Alba
Domínguez González, Mayelín
Ayala, Victòria
Jove, Mariona
Mota-Martorell, Natalia
Piñol Ripoll, Gerard
Gil-Villar, Maria Pilar
Rué, Montserrat
Portero-Otin, Manuel
Ferrer, Isidro (Ferrer Abizanda)
Pamplona, Reinald
author2_role author
author
author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Envelliment
Lòbul frontal
Metabolisme
Aging
Frontal lobe
Metabolism
topic Envelliment
Lòbul frontal
Metabolisme
Aging
Frontal lobe
Metabolism
description Human 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.
publishDate 2017
dc.date.none.fl_str_mv 2017
2019
2019
2019
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/acceptedVersion
format article
status_str acceptedVersion
dc.identifier.none.fl_str_mv https://hdl.handle.net/2445/140516
url https://hdl.handle.net/2445/140516
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.relation.none.fl_str_mv Versió postprint del document publicat a: https://doi.org/10.1016/j.freeradbiomed.2016.12.010
Free Radical Biology and Medicine, 2017, vol. 103, p. 14-22
https://doi.org/10.1016/j.freeradbiomed.2016.12.010
dc.rights.none.fl_str_mv cc-by-nc-nd (c) Elsevier B.V., 2017
http://creativecommons.org/licenses/by-nc-nd/3.0/es
info:eu-repo/semantics/openAccess
rights_invalid_str_mv cc-by-nc-nd (c) Elsevier B.V., 2017
http://creativecommons.org/licenses/by-nc-nd/3.0/es
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv 9 p.
application/pdf
dc.publisher.none.fl_str_mv Elsevier B.V.
publisher.none.fl_str_mv Elsevier B.V.
dc.source.none.fl_str_mv Articles publicats en revistes (Patologia i Terapèutica Experimental)
reponame:Recercat. Dipósit de la Recerca de Catalunya
instname:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
instname_str Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
reponame_str Recercat. Dipósit de la Recerca de Catalunya
collection Recercat. Dipósit de la Recerca de Catalunya
repository.name.fl_str_mv
repository.mail.fl_str_mv
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score 15,81155

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