Plasma and cerebrospinal fluid nonenzymatic protein damage is sustained in Alzheimer's disease

Background Oxidative stress is considered to play an important role in the pathogenesis of Alzheimer's disease (AD). It has been observed that oxidative damage to specific protein targets affecting particular functional networks is one of the mechanisms by which oxidative stress contributes to...

Descripción completa

Detalles Bibliográficos
Autores: Dakterzada, Farida, Jové Font, Mariona, Cantero, José Luís, Pamplona Gras, Reinald
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2023
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:10459.1/464233
Acceso en línea:https://doi.org/10.1016/j.redox.2023.102772
https://hdl.handle.net/10459.1/464233
Access Level:acceso abierto
Palabra clave:Advanced glycation end-products
Advanced lipoxidation end-products
Alzheimer's disease
Mild cognitive impairment
Cerebrospinal fluid
Plasma
Protein oxidation
id ES_cb40ed5a68a288759d5df69bcbdfd53c
oai_identifier_str oai:recercat.cat:10459.1/464233
network_acronym_str ES
network_name_str España
repository_id_str
dc.title.none.fl_str_mv Plasma and cerebrospinal fluid nonenzymatic protein damage is sustained in Alzheimer's disease
title Plasma and cerebrospinal fluid nonenzymatic protein damage is sustained in Alzheimer's disease
spellingShingle Plasma and cerebrospinal fluid nonenzymatic protein damage is sustained in Alzheimer's disease
Dakterzada, Farida
Advanced glycation end-products
Advanced lipoxidation end-products
Alzheimer's disease
Mild cognitive impairment
Cerebrospinal fluid
Plasma
Protein oxidation
title_short Plasma and cerebrospinal fluid nonenzymatic protein damage is sustained in Alzheimer's disease
title_full Plasma and cerebrospinal fluid nonenzymatic protein damage is sustained in Alzheimer's disease
title_fullStr Plasma and cerebrospinal fluid nonenzymatic protein damage is sustained in Alzheimer's disease
title_full_unstemmed Plasma and cerebrospinal fluid nonenzymatic protein damage is sustained in Alzheimer's disease
title_sort Plasma and cerebrospinal fluid nonenzymatic protein damage is sustained in Alzheimer's disease
dc.creator.none.fl_str_mv Dakterzada, Farida
Jové Font, Mariona
Cantero, José Luís
Pamplona Gras, Reinald
author Dakterzada, Farida
author_facet Dakterzada, Farida
Jové Font, Mariona
Cantero, José Luís
Pamplona Gras, Reinald
author_role author
author2 Jové Font, Mariona
Cantero, José Luís
Pamplona Gras, Reinald
author2_role author
author
author
dc.subject.none.fl_str_mv Advanced glycation end-products
Advanced lipoxidation end-products
Alzheimer's disease
Mild cognitive impairment
Cerebrospinal fluid
Plasma
Protein oxidation
topic Advanced glycation end-products
Advanced lipoxidation end-products
Alzheimer's disease
Mild cognitive impairment
Cerebrospinal fluid
Plasma
Protein oxidation
description Background Oxidative stress is considered to play an important role in the pathogenesis of Alzheimer's disease (AD). It has been observed that oxidative damage to specific protein targets affecting particular functional networks is one of the mechanisms by which oxidative stress contributes to neuronal failure and consequently loss of cognition and AD progression. Studies are lacking in which oxidative damage is measured at both systemic and central fluid levels and in the same cohort of patients. We aimed to determine the levels of both plasma and cerebrospinal fluid (CSF) nonenzymatic protein damage in patients in the continuum of AD and to evaluate the relation of this damage with clinical progression from mild cognitive impairment (MCI) to AD. Methods Different markers of nonenzymatic post-translational protein modification, mostly from oxidative processes, were detected and quantified in plasma and CSF by isotope dilution gas chromatography‒mass spectrometry using selected ion monitoring (SIM-GC/MS) for 289 subjects: 103 AD, 92 MCI, and 94 control subjects. Characteristics of the study population such as age, sex, Mini-mental state examination, CSF AD biomarkers, and APOE ϵ4, were also considered. Results Forty-seven (52.8%) MCI patients progressed to AD during follow-up (58 ± 12.5 months). After controlling for age, sex, and APOE ϵ4 allele, plasma and CSF concentrations of protein damage markers were not associated with either diagnosis of AD or MCI. The CSF levels of nonenzymatic protein damage markers were associated with none of the CSF AD biomarkers. In addition, neither in CSF nor in plasma were the levels of protein damage associated with the MCI to AD progression. Conclusion The lack of association between both CSF and plasma concentrations of nonenzymatic protein damage markers and AD diagnosis and progression suggests that oxidative damage in AD is a pathogenic mechanism specifically expressed at the cell-tissue level, not in extracellular fluids.
publishDate 2023
dc.date.none.fl_str_mv 2023
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv https://doi.org/10.1016/j.redox.2023.102772
https://hdl.handle.net/10459.1/464233
url https://doi.org/10.1016/j.redox.2023.102772
https://hdl.handle.net/10459.1/464233
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.relation.none.fl_str_mv info:eu-repo/grantAgreement/AEI/Plan Estatal de Investigación Científica y Técnica y de Innovación 2017-2020/RTI2018-099200-B-I00
info:eu-repo/grantAgreement/AEI/Plan Estatal de Investigación Científica, Técnica y de Innovación 2021-2023/PID2022-143140OB-I00
info:eu-repo/grantAgreement/AEI/Plan Estatal de Investigación Científica y Técnica y de Innovación 2017-2020/PID2020-119978RB-I00
Reproducció del document publicat a https://doi.org/10.1016/j.redox.2023.102772
Redox Biology, 2023, vol. 64, 102772
dc.rights.none.fl_str_mv cc-by-nc-nd (c) Farida Dakterzada et al., 2023
Attribution-NonCommercial-NoDerivatives 4.0 International
info:eu-repo/semantics/openAccess
http://creativecommons.org/licenses/by-nc-nd/4.0/
rights_invalid_str_mv cc-by-nc-nd (c) Farida Dakterzada et al., 2023
Attribution-NonCommercial-NoDerivatives 4.0 International
http://creativecommons.org/licenses/by-nc-nd/4.0/
eu_rights_str_mv openAccess
dc.publisher.none.fl_str_mv Elsevier
publisher.none.fl_str_mv Elsevier
dc.source.none.fl_str_mv 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
_version_ 1869419572348583936
spelling Plasma and cerebrospinal fluid nonenzymatic protein damage is sustained in Alzheimer's diseaseDakterzada, FaridaJové Font, MarionaCantero, José LuísPamplona Gras, ReinaldAdvanced glycation end-productsAdvanced lipoxidation end-productsAlzheimer's diseaseMild cognitive impairmentCerebrospinal fluidPlasmaProtein oxidationBackground Oxidative stress is considered to play an important role in the pathogenesis of Alzheimer's disease (AD). It has been observed that oxidative damage to specific protein targets affecting particular functional networks is one of the mechanisms by which oxidative stress contributes to neuronal failure and consequently loss of cognition and AD progression. Studies are lacking in which oxidative damage is measured at both systemic and central fluid levels and in the same cohort of patients. We aimed to determine the levels of both plasma and cerebrospinal fluid (CSF) nonenzymatic protein damage in patients in the continuum of AD and to evaluate the relation of this damage with clinical progression from mild cognitive impairment (MCI) to AD. Methods Different markers of nonenzymatic post-translational protein modification, mostly from oxidative processes, were detected and quantified in plasma and CSF by isotope dilution gas chromatography‒mass spectrometry using selected ion monitoring (SIM-GC/MS) for 289 subjects: 103 AD, 92 MCI, and 94 control subjects. Characteristics of the study population such as age, sex, Mini-mental state examination, CSF AD biomarkers, and APOE ϵ4, were also considered. Results Forty-seven (52.8%) MCI patients progressed to AD during follow-up (58 ± 12.5 months). After controlling for age, sex, and APOE ϵ4 allele, plasma and CSF concentrations of protein damage markers were not associated with either diagnosis of AD or MCI. The CSF levels of nonenzymatic protein damage markers were associated with none of the CSF AD biomarkers. In addition, neither in CSF nor in plasma were the levels of protein damage associated with the MCI to AD progression. Conclusion The lack of association between both CSF and plasma concentrations of nonenzymatic protein damage markers and AD diagnosis and progression suggests that oxidative damage in AD is a pathogenic mechanism specifically expressed at the cell-tissue level, not in extracellular fluids.This research was supported by the Government of Catalonia, Department of Health (PERIS 2019 SLT008/18/00050), and the Agency for the Management of University and Research Grants (2021SGR 00761) to GPR. The spanish Ministry of Science, Innovation, and Universities (grant RTI2018-099200-B-I00 and PID2022-143140OB-I00), the Diputacio ´ de Lleida (PP10605 - PIRS2021), and the Generalitat of Catalonia: Agency for Management of University and Research Grants (2021SGR00990) and Department of Health (SLT002/16/00250) to RP. The Spanish Ministry of Economy and Competitiveness (PID2020-119978RB-I00), CIBERNED, Alzheimer’s Association (AARG-NTF-22- 924702), the Junta de Andalucía (PY20_00858), and the AndalucíaFEDER Program (UPO-1380913) to JLC. This study has been co-financed by FEDER funds from the European Union (“A way to build Europe”). IRBLleida is a CERCA Programme/Generalitat of Catalonia.Elsevier2023info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttps://doi.org/10.1016/j.redox.2023.102772https://hdl.handle.net/10459.1/464233reponame:Recercat. Dipósit de la Recerca de Catalunyainstname:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)Inglésinfo:eu-repo/grantAgreement/AEI/Plan Estatal de Investigación Científica y Técnica y de Innovación 2017-2020/RTI2018-099200-B-I00info:eu-repo/grantAgreement/AEI/Plan Estatal de Investigación Científica, Técnica y de Innovación 2021-2023/PID2022-143140OB-I00info:eu-repo/grantAgreement/AEI/Plan Estatal de Investigación Científica y Técnica y de Innovación 2017-2020/PID2020-119978RB-I00Reproducció del document publicat a https://doi.org/10.1016/j.redox.2023.102772Redox Biology, 2023, vol. 64, 102772cc-by-nc-nd (c) Farida Dakterzada et al., 2023Attribution-NonCommercial-NoDerivatives 4.0 Internationalinfo:eu-repo/semantics/openAccesshttp://creativecommons.org/licenses/by-nc-nd/4.0/oai:recercat.cat:10459.1/4642332026-05-29T05:05:01Z
score 15,81155

Similares en LA Referencia