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Olfactory bulb neuroproteomics reveals a chronological perturbation of survival routes and a disruption of prohibitin complex during Alzheimer's disease progression
dc.creator | Lachén Montes, Mercedes | es_ES |
dc.creator | González Morales, Andrea | es_ES |
dc.creator | Zelaya Huerta, María Victoria | es_ES |
dc.creator | Pérez Valderrama, Estela | es_ES |
dc.creator | Ausín, Karina | es_ES |
dc.creator | Ferrer, Isidro | es_ES |
dc.creator | Fernández Irigoyen, Joaquín | es_ES |
dc.creator | Santamaría, Enrique | es_ES |
dc.date.accessioned | 2018-09-19T09:37:47Z | |
dc.date.available | 2018-09-19T09:37:47Z | |
dc.date.issued | 2017 | |
dc.identifier.issn | 2045-2322 (Electronic) | |
dc.identifier.uri | https://hdl.handle.net/2454/30733 | |
dc.description.abstract | Olfactory dysfunction is among the earliest features of Alzheimer’s disease (AD). Although neuropathological abnormalities have been detected in the olfactory bulb (OB), little is known about its dynamic biology. Here, OB- proteome analysis showed a stage-dependent synaptic proteostasis impairment during AD evolution. In addition to progressive modulation of tau and amyloid precursor protein (APP) interactomes, network-driven proteomics revealed an early disruption of upstream and downstream p38 MAPK pathway and a subsequent impairment of Phosphoinositide-dependent protein kinase 1 (PDK1)/Protein kinase C (PKC) signaling axis in the OB from AD subjects. Moreover, a mitochondrial imbalance was evidenced by a depletion of Prohibitin-2 (Phb2) levels and a specific decrease in the phosphorylated isoforms of Phb1 in intermediate and advanced AD stages. Interestingly, olfactory Phb subunits were also deregulated across different types of dementia. Phb2 showed a specific up-regulation in mixed dementia, while Phb1 isoforms were down-regulated in frontotemporal lobar degeneration (FTLD). However, no differences were observed in the olfactory expression of Phb subunits in progressive supranuclear palsy (PSP). To sum up, our data reflect, in part, the missing links in the biochemical understanding of olfactory dysfunction in AD, unveiling Phb complex as a differential driver of neurodegeneration at olfactory level. | en |
dc.description.sponsorship | This work was funded by grants from the Spanish Ministry of Economy and Competitiveness (MINECO) (Ref. SAF2014-59340-R), Department of Economic Development from Government of Navarra (Ref. PC025), and Obra Social la Caixa to ES. AGM and KA are supported by PEJ-2014-A-61949 and PEJ-2014-A-72151 (MINECO). EPV is supported by PTA-2013/8711/I (MINECO). MLM is supported by a predoctoral fellowship from the Public University of Navarra (UPNA). The Proteomics Unit of Navarrabiomed is a member of Proteored, PRB2-ISCIII, and is supported by grant PT13/0001, of the PE I + D + I 2013-2016 funded by ISCIII and FEDER. | en |
dc.format.extent | 15 p. | |
dc.format.mimetype | application/pdf | en |
dc.format.mimetype | application/zip | en |
dc.language.iso | eng | en |
dc.publisher | Springer Nature | en |
dc.relation.ispartof | Scientific Reports, 7: 9115 | en |
dc.rights | This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. | en |
dc.rights.uri | https://creativecommons.org/licenses/by/4.0/ | |
dc.subject | Health | en |
dc.subject | Radio planning | en |
dc.title | Olfactory bulb neuroproteomics reveals a chronological perturbation of survival routes and a disruption of prohibitin complex during Alzheimer's disease progression | en |
dc.type | info:eu-repo/semantics/article | en |
dc.type | Artículo / Artikulua | es |
dc.contributor.department | Ciencias de la Salud | es_ES |
dc.contributor.department | Osasun Zientziak | eu |
dc.rights.accessRights | info:eu-repo/semantics/openAccess | en |
dc.rights.accessRights | Acceso abierto / Sarbide irekia | es |
dc.identifier.doi | 10.1038/s41598-017-09481-x | |
dc.relation.projectID | info:eu-repo/grantAgreement/MINECO//SAF2014-59340-R/ES/ | en |
dc.relation.publisherversion | https://doi.org/10.1038/s41598-017-09481-x | |
dc.type.version | info:eu-repo/semantics/publishedVersion | en |
dc.type.version | Versión publicada / Argitaratu den bertsioa | es |
dc.contributor.funder | Gobierno de Navarra / Nafarroako Gobernua, PC025 | es |
dc.contributor.funder | Universidad Pública de Navarra / Nafarroako Unibertsitate Publikoa | es |
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