The CSF p-tau/ß-amyloid 42 ratio correlates with brain structure and fibrillary ß-amyloid deposition in cognitively unimpaired individuals at the earliest stages of pre-clinical Alzheimer's disease

CSF concentrations of β-amyloid 42 (Aβ42) and phosphorylated tau (p-tau) are well-established biomarkers of Alzheimer's disease and have been studied in relation to several neuropathological features both in patients and in cognitively unimpaired individuals. The CSF p-tau/Aβ42 ratio, a biomark...

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Autores: Cacciaglia, Raffaele, Shekari, Mahnaz, Salvadó, Gemma, Milà Alomà, Marta, Falcón, Carles, Sánchez Benavides, Gonzalo, Minguillón, Carolina, Fauria, Karine, Grau-Rivera, Oriol, Molinuevo, José Luis, Blennow, Kaj, Zetterberg, Henrik, Quevenco, Frances-Catherine, Suárez-Calvet, Marc, Gispert López, Juan Domingo, ALFA Study
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2024
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:10230/71640
Acceso en línea:http://hdl.handle.net/10230/71640
http://dx.doi.org/10.1093/braincomms/fcae451
Access Level:acceso abierto
Palabra clave:Alzheimer's disease
CSF biomarkers
Amyloid deposition
Brain structure
p-tau/Aß42 ratio
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dc.title.none.fl_str_mv The CSF p-tau/ß-amyloid 42 ratio correlates with brain structure and fibrillary ß-amyloid deposition in cognitively unimpaired individuals at the earliest stages of pre-clinical Alzheimer's disease
title The CSF p-tau/ß-amyloid 42 ratio correlates with brain structure and fibrillary ß-amyloid deposition in cognitively unimpaired individuals at the earliest stages of pre-clinical Alzheimer's disease
spellingShingle The CSF p-tau/ß-amyloid 42 ratio correlates with brain structure and fibrillary ß-amyloid deposition in cognitively unimpaired individuals at the earliest stages of pre-clinical Alzheimer's disease
Cacciaglia, Raffaele
Alzheimer's disease
CSF biomarkers
Amyloid deposition
Brain structure
p-tau/Aß42 ratio
title_short The CSF p-tau/ß-amyloid 42 ratio correlates with brain structure and fibrillary ß-amyloid deposition in cognitively unimpaired individuals at the earliest stages of pre-clinical Alzheimer's disease
title_full The CSF p-tau/ß-amyloid 42 ratio correlates with brain structure and fibrillary ß-amyloid deposition in cognitively unimpaired individuals at the earliest stages of pre-clinical Alzheimer's disease
title_fullStr The CSF p-tau/ß-amyloid 42 ratio correlates with brain structure and fibrillary ß-amyloid deposition in cognitively unimpaired individuals at the earliest stages of pre-clinical Alzheimer's disease
title_full_unstemmed The CSF p-tau/ß-amyloid 42 ratio correlates with brain structure and fibrillary ß-amyloid deposition in cognitively unimpaired individuals at the earliest stages of pre-clinical Alzheimer's disease
title_sort The CSF p-tau/ß-amyloid 42 ratio correlates with brain structure and fibrillary ß-amyloid deposition in cognitively unimpaired individuals at the earliest stages of pre-clinical Alzheimer's disease
dc.creator.none.fl_str_mv Cacciaglia, Raffaele
Shekari, Mahnaz
Salvadó, Gemma
Milà Alomà, Marta
Falcón, Carles
Sánchez Benavides, Gonzalo
Minguillón, Carolina
Fauria, Karine
Grau-Rivera, Oriol
Molinuevo, José Luis
Blennow, Kaj
Zetterberg, Henrik
Quevenco, Frances-Catherine
Suárez-Calvet, Marc
Gispert López, Juan Domingo
ALFA Study
author Cacciaglia, Raffaele
author_facet Cacciaglia, Raffaele
Shekari, Mahnaz
Salvadó, Gemma
Milà Alomà, Marta
Falcón, Carles
Sánchez Benavides, Gonzalo
Minguillón, Carolina
Fauria, Karine
Grau-Rivera, Oriol
Molinuevo, José Luis
Blennow, Kaj
Zetterberg, Henrik
Quevenco, Frances-Catherine
Suárez-Calvet, Marc
Gispert López, Juan Domingo
ALFA Study
author_role author
author2 Shekari, Mahnaz
Salvadó, Gemma
Milà Alomà, Marta
Falcón, Carles
Sánchez Benavides, Gonzalo
Minguillón, Carolina
Fauria, Karine
Grau-Rivera, Oriol
Molinuevo, José Luis
Blennow, Kaj
Zetterberg, Henrik
Quevenco, Frances-Catherine
Suárez-Calvet, Marc
Gispert López, Juan Domingo
ALFA Study
author2_role author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Alzheimer's disease
CSF biomarkers
Amyloid deposition
Brain structure
p-tau/Aß42 ratio
topic Alzheimer's disease
CSF biomarkers
Amyloid deposition
Brain structure
p-tau/Aß42 ratio
description CSF concentrations of β-amyloid 42 (Aβ42) and phosphorylated tau (p-tau) are well-established biomarkers of Alzheimer's disease and have been studied in relation to several neuropathological features both in patients and in cognitively unimpaired individuals. The CSF p-tau/Aβ42 ratio, a biomarker combining information from both pathophysiological processes, has emerged as a promising tool for monitoring disease progression, even at pre-clinical stages. Here, we studied the association between the CSF p-tau/Aβ42 ratio with downstream markers of pre-clinical Alzheimer's disease progression including brain structure, glucose metabolism, fibrillary Aβ deposition and cognitive performance in 234 cognitively unimpaired individuals, who underwent cognitive testing, a lumbar puncture, MRI, 18F-fluorodeoxyglucose and 18F-flutemetamol PET scanning. We evaluated both main effects and interactions with Alzheimer's disease risk factors, such as older age, female sex and the apoliporoptein E (APOE)-ɛ4 allele, in a priori defined regions of interest and further examined the associations on the whole-brain using voxel-wise regressions. In addition, as the association between CSF Alzheimer's disease biomarkers and brain structure and function may be non-linear, we tested the interaction between the CSF p-tau/Aβ42 ratio and stages of pre-clinical Alzheimer's disease defined using the amyloid (A) and tau (T) classification. We found significantly positive associations between CSF p-tau/Aβ42 and both cortical Aβ deposition and regional grey matter volume while no effect was observed for brain metabolism. A significant interaction with age indicated that, for the same level of CSF p-tau/Aβ42, older individuals displayed both increased Aβ deposition and lower grey matter volume, in widespread cortical areas. In addition, we found that women compared with men had a greater Aβ fibrillary accumulation in midline cortical areas and inferior temporal regions, for the same level of the CSF biomarker. The impact of CSF p-tau/Aβ42 on grey matter volume was modulated by AT stages, with A+T+ individuals displaying significantly less positive associations in areas of early atrophy in the Alzheimer's continuum. Finally, we found that sex and APOE-ɛ4 modulated the association between the CSF biomarker and episodic memory as well as abstract reasoning, respectively. Our data indicate that the CSF p-tau/Aβ42 ratio is strongly associated with multiple downstream neuropathological events in cognitively unimpaired individuals and may thus serve as a potent biomarker to investigate the earliest changes in pre-clinical Alzheimer's disease. Given that its impact on both Aβ deposition and grey matter volume is modulated by specific risk factors, our results highlight the need to take into account such predisposing variables in both clinical practice and prevention trials.
publishDate 2024
dc.date.none.fl_str_mv 2024
2025
2025
2025
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 http://hdl.handle.net/10230/71640
http://dx.doi.org/10.1093/braincomms/fcae451
http://hdl.handle.net/10230/71640
url http://hdl.handle.net/10230/71640
http://dx.doi.org/10.1093/braincomms/fcae451
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.relation.none.fl_str_mv Brain Communications. 2024;7(1)
info:eu-repo/grantAgreement/ES/3PE/PID2021-125433OA-100
info:eu-repo/grantAgreement/EC/HE/101053962
info:eu-repo/grantAgreement/EC/H2020/860197
info:eu-repo/grantAgreement/EC/H2020/948677
info:eu-repo/grantAgreement/EC/H2020/847648
dc.rights.none.fl_str_mv http://creativecommons.org/licenses/by/4.0/
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eu_rights_str_mv openAccess
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dc.publisher.none.fl_str_mv Oxford University Press
publisher.none.fl_str_mv Oxford University Press
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
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spelling The CSF p-tau/ß-amyloid 42 ratio correlates with brain structure and fibrillary ß-amyloid deposition in cognitively unimpaired individuals at the earliest stages of pre-clinical Alzheimer's diseaseCacciaglia, RaffaeleShekari, MahnazSalvadó, GemmaMilà Alomà, MartaFalcón, CarlesSánchez Benavides, GonzaloMinguillón, CarolinaFauria, KarineGrau-Rivera, OriolMolinuevo, José LuisBlennow, KajZetterberg, HenrikQuevenco, Frances-CatherineSuárez-Calvet, MarcGispert López, Juan DomingoALFA StudyAlzheimer's diseaseCSF biomarkersAmyloid depositionBrain structurep-tau/Aß42 ratioCSF concentrations of β-amyloid 42 (Aβ42) and phosphorylated tau (p-tau) are well-established biomarkers of Alzheimer's disease and have been studied in relation to several neuropathological features both in patients and in cognitively unimpaired individuals. The CSF p-tau/Aβ42 ratio, a biomarker combining information from both pathophysiological processes, has emerged as a promising tool for monitoring disease progression, even at pre-clinical stages. Here, we studied the association between the CSF p-tau/Aβ42 ratio with downstream markers of pre-clinical Alzheimer's disease progression including brain structure, glucose metabolism, fibrillary Aβ deposition and cognitive performance in 234 cognitively unimpaired individuals, who underwent cognitive testing, a lumbar puncture, MRI, 18F-fluorodeoxyglucose and 18F-flutemetamol PET scanning. We evaluated both main effects and interactions with Alzheimer's disease risk factors, such as older age, female sex and the apoliporoptein E (APOE)-ɛ4 allele, in a priori defined regions of interest and further examined the associations on the whole-brain using voxel-wise regressions. In addition, as the association between CSF Alzheimer's disease biomarkers and brain structure and function may be non-linear, we tested the interaction between the CSF p-tau/Aβ42 ratio and stages of pre-clinical Alzheimer's disease defined using the amyloid (A) and tau (T) classification. We found significantly positive associations between CSF p-tau/Aβ42 and both cortical Aβ deposition and regional grey matter volume while no effect was observed for brain metabolism. A significant interaction with age indicated that, for the same level of CSF p-tau/Aβ42, older individuals displayed both increased Aβ deposition and lower grey matter volume, in widespread cortical areas. In addition, we found that women compared with men had a greater Aβ fibrillary accumulation in midline cortical areas and inferior temporal regions, for the same level of the CSF biomarker. The impact of CSF p-tau/Aβ42 on grey matter volume was modulated by AT stages, with A+T+ individuals displaying significantly less positive associations in areas of early atrophy in the Alzheimer's continuum. Finally, we found that sex and APOE-ɛ4 modulated the association between the CSF biomarker and episodic memory as well as abstract reasoning, respectively. Our data indicate that the CSF p-tau/Aβ42 ratio is strongly associated with multiple downstream neuropathological events in cognitively unimpaired individuals and may thus serve as a potent biomarker to investigate the earliest changes in pre-clinical Alzheimer's disease. Given that its impact on both Aβ deposition and grey matter volume is modulated by specific risk factors, our results highlight the need to take into account such predisposing variables in both clinical practice and prevention trials.The research leading to these results has received funding from ‘la Caixa’ Foundation (ID 100010434), under agreement LCF/PR/GN17/50300004 and the Alzheimer’s Association and an international anonymous charity foundation through the TriBEKa Imaging Platform project (TriBEKa-17-519007). Additional support has been received from the Universities and Research Secretariat, Ministry of Business and Knowledge of the Catalan Government under the grant no. 2021 SGR 00913. R.C. receives funding from ‘Ministerio de Ciencia, Innovación y Universidades—Agencia Estatal de Investigación’ MCIN/AEI/10.13039/501100011033/FEDER, EU, through project PID2021-125433OA-100 and support from grant RYC2021-031128-I, funded by MCIN/AEI/10.13039/501100011033 and the European Union NextGenerationEU/Plan de Recuperación, Transformación y Resiliencia (PRTR). H.Z. is a Wallenberg Scholar supported by grants from the Swedish Research Council (#2018-02532), the European Union’s Horizon Europe research and innovation programme under grant agreement no. 101053962, Swedish State Support for Clinical Research (#ALFGBG-71320), the Alzheimer Drug Discovery Foundation (ADDF), USA (#201809-2016862), the AD Strategic Fund and the Alzheimer’s Association (#ADSF-21-831376-C, #ADSF-21-831381-C and #ADSF-21-831377-C), the Bluefield Project, the Olav Thon Foundation, the Erling-Persson Family Foundation, Stiftelsen för Gamla Tjänarinnor, Hjärnfonden, Sweden (#FO2022-0270), the European Union’s Horizon 2020 research and innovation programme under the Marie Skłodowska-Curie grant agreement no. 860197 (MIRIADE), the European Union Joint Programme—Neurodegenerative Disease Research (JPND2021-00694) and the UK Dementia Research Institute at University College London (UCL) (UKDRI-1003). K.B. is supported by the Swedish Research Council (#2017-00915), the Alzheimer Drug Discovery Foundation (ADDF), USA (#RDAPB-201809-2016615), the Swedish Alzheimer Foundation (#AF-930351, #AF-939721 and #AF-968270), Hjärnfonden, Sweden (#FO2017-0243 and #ALZ2022-0006), the Swedish state under the agreement between the Swedish government and the County Councils, the Avtal om Läkarutbildning och Forskning (ALF) agreement (#ALFGBG-715986 and #ALFGBG-965240), the European Union Joint Programme for Neurodegenerative Disorders (JPND2019-466-236), the National Institutes of Health (NIH), USA, (grant #1R01AG068398-01), the Alzheimer’s Association 2021 Zenith Award (ZEN-21-848495) and the Alzheimer’s Association 2022–25 Grant (SG-23-1038904 QC). M.S.-C. receives funding from the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation programme (grant agreement no. 948677), Project ‘PI19/00155’, funded by Instituto de Salud Carlos III (ISCIII) and co-funded by the European Union and from a fellowship from ‘la Caixa’ Foundation (ID 100010434) and from the European Union’s Horizon 2020 research and innovation programme under the Marie Skłodowska-Curie grant agreement no. 847648 (LCF/BQ/PR21/11840004). O.G.-R. is supported by the ‘Ministerio de Ciencia, Innovación y Universidades' (IJC2020-043417-I) and receives funding from the Alzheimer’s Association (2019-AARF-644568) and the Instituto de Salud Carlos III (PI19/00117).Oxford University Press2025202520242025info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfapplication/pdfhttp://hdl.handle.net/10230/71640http://dx.doi.org/10.1093/braincomms/fcae451http://hdl.handle.net/10230/71640reponame:Recercat. Dipósit de la Recerca de Catalunyainstname:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)InglésBrain Communications. 2024;7(1)info:eu-repo/grantAgreement/ES/3PE/PID2021-125433OA-100info:eu-repo/grantAgreement/EC/HE/101053962info:eu-repo/grantAgreement/EC/H2020/860197info:eu-repo/grantAgreement/EC/H2020/948677info:eu-repo/grantAgreement/EC/H2020/847648© The Author(s) 2024. Published by Oxford University Press on behalf of the Guarantors of Brain. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.http://creativecommons.org/licenses/by/4.0/info:eu-repo/semantics/openAccessoai:recercat.cat:10230/716402026-05-29T05:05:01Z
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