SCD-plus features and AD biomarkers in cognitively unimpaired samples: A meta-analytic approach for nine cohort studies

  • Alzheimer's Disease Neuroimaging Initiative
  • , the Australian Imaging Biomarkers and Lifestyle Flagship Study of Ageing
  • , A4 Study team, full listing of team and site personnel available at A4STUDΥ.org
  • , DELCODE study
  • , Harvard Aging Brain Study

Research output: Contribution to JournalArticleAcademicpeer-review

Abstract

Introduction: Specific features of subjective cognitive decline (SCD-plus) have been proposed to indicate an increased risk of preclinical Alzheimer's disease (AD). However, few studies have examined how these features relate to AD biomarkers in cognitively unimpaired (CU) older adults.

Methods: Meta-analyses were performed using cross-sectional data from nine cohorts (n = 7219, mean age (SD): 71.17 (5.9), 56.5% female) to determine associations of SCD-plus features with positron emission tomography (PET)- or cerebrospinal fluid (CSF)-derived amyloid beta (Aβ) and tau biomarkers.

Results: Participants with preclinical AD (community-based only) were more likely to fulfill SCD-plus features. The presence of self-reported memory decline, associated concern/worry, and a higher number of fulfilled features were all associated with high Aβ levels. Only the latter was associated with abnormal tau.

Discussion: Simultaneous endorsement of multiple SCD-plus features is a robust indicator of abnormal AD biomarkers in CU older adults, whereas isolated SCD features seem only sensitive to elevated Aβ, supporting their value as early behavioral markers of preclinical AD.

Highlights: About two-tenths of our sample had abnormal amyloid beta (Aβ) levels with evidence of subjective cognitive decline (SCD). Preclinical AD subsamples (community-based) had a higher percentage of participants meeting SCD-plus features. Self-reported memory decline and concern/worry were the sole features associated with high Aβ, but not tau, burden. A higher number of fulfilled SCD-plus features are linked to high Aβ and tau burden. Use of multiple SCD-plus features may help identify early stages of biological AD.
Original languageEnglish
Article numbere14307
Pages (from-to)1-17
Number of pages17
JournalAlzheimer's & dementia : the journal of the Alzheimer's Association
Volume21
Issue number5
Early online date22 Feb 2025
DOIs
Publication statusPublished - May 2025

Funding

This manuscript was facilitated by the Alzheimer's Association International Society to Advance Alzheimer's Research and Treatment (ISTAART), through the Subjective Cognitive Decline professional interest area (PIA). The views and opinions expressed by authors in this publication represent those of the authors and do not necessarily reflect those of the PIA membership, ISTAART or the Alzheimer's Association. Elizabeth Kuhn was funded by the University of Caen Normandy, INSERM, the Fondation Philippe Chatrier and the Helmholtz Association's Initiative and Networking Fund through Helmholtz Artificial Intelligence Cooperation Unit (ZT-I-PF-5-163). Rachel Buckley is funded by a NIH Pathway to Independence award, R00-AG061238, an NIH New Innovator award, DP2AG082342, and an R01-AG079142. Katherine A. Gifford was funded by a K23-AG045966 and R01-AG062826. Gonzalo Sánchez Benavides is supported by Instituto de Salud Carlos III (ISCIII) through the project CP23/00039 (Miguel Servet contract), co-funded by the European Union (FSE+). *Part of the data used in preparation of this article was obtained from the Alzheimer's Disease Neuroimaging Initiative (ADNI) database (https://adni.loni.usc.edu) As such, the investigators within the ADNI contributed to the design and implementation of ADNI and/or provided data, but they did not participate in analysis or writing of this report. A complete listing of ADNI investigators can be found at: http://adni.loni.usc.edu/wpcontent/uploads/how_to_apply/ADNI_Acknowledgement_List.pdf. The ADNI was launched in 2003 as a public-private partnership led by Principal Investigator Michael W. Weiner, MD. The primary goal of ADNI has been to test whether serial magnetic resonance imaging (MRI), positron emission tomography (PET), other biological markers, and clinical and neuropsychological assessment can be combined to measure the progression of mild cognitive impairment (MCI) and early Alzheimer's disease (AD). *ADNI data collection and sharing for this project was funded by the ADNI (National Institutes of Health Grant U01 AG024904) and DOD ADNI (Department of Defense award number W81XWH-12-2-0012). ADNI is funded by the National Institute on Aging, the National Institute of Biomedical Imaging and Bioengineering, and through generous contributions from the following: AbbVie, Alzheimer's Association; Alzheimer's Drug Discovery Foundation; Araclon Biotech; BioClinica, Inc.; Biogen; Bristol-Myers Squibb Company; CereSpir, Inc.; Cogstate; Eisai Inc.; Elan Pharmaceuticals, Inc.; Eli Lilly and Company; EuroImmun; F. Hoffmann-La Roche Ltd and its affiliated company Genentech, Inc.; Fujirebio; GE Healthcare; IXICO Ltd.; Janssen Alzheimer Immunotherapy Research & Development, LLC.; Johnson & Johnson Pharmaceutical Research & Development LLC.; Lumosity; Lundbeck; Merck & Co., Inc.; Meso Scale Diagnostics, LLC.; NeuroRx Research; Neurotrack Technologies; Novartis Pharmaceuticals Corporation; Pfizer Inc.; Piramal Imaging; Servier; Takeda Pharmaceutical Company; and Transition Therapeutics. The Canadian Institutes of Health Research is providing funds to support ADNI clinical sites in Canada. Private sector contributions are facilitated by the Foundation for the National Institutes of Health (www.fnih.org). The grantee organization is the Northern California Institute for Research and Education, and the study is coordinated by the Alzheimer's Therapeutic Research Institute at the University of Southern California. ADNI data are disseminated by the Laboratory for Neuro Imaging at the University of Southern California. Part of the data used in the preparation of this article was obtained from the Australian Imaging Biomarkers and Lifestyle flagship study of ageing (AIBL) which was made available at the ADNI database (www.loni.usc.edu/ADNI). The AIBL researchers contributed data but did not participate in analysis or writing of this report. AIBL researchers are listed at www.aibl.csiro.au. The AIBL study www.AIBL.csiro.au is a consortium between Austin Health, Commonwealth Scientific and Industrial Research Organisation (CSIRO), Edith Cowan University, the Florey Institute (The University of Melbourne), and the National Ageing Research Institute. **Part of data used in the preparation of this article were obtained from the A4 Study (https://a4study.org/) is a secondary prevention trial in preclinical Alzheimer's disease, aiming to slow cognitive decline associated with brain amyloid accumulation in clinically normal older individuals. The A4 and LEARN Studies are led by Dr. Reisa Sperling at Brigham and Women's Hospital, Harvard Medical School and Dr. Paul Aisen at the Alzheimer's Therapeutic Research Institute (ATRI), University of Southern California. The A4 and LEARN Studies are coordinated by ATRI at the University of Southern California, and the data are made available through the Laboratory for Neuro Imaging at the University of Southern California. The participants screening for the A4 Study provided permission to share their de-identified data in order to advance the quest to find a successful treatment for Alzheimer's disease. We would like to acknowledge the dedication of all the participants, the site personnel, and all of the partnership team members who continue to make the A4 and LEARN Studies possible. The complete A4 Study Team list is available on: http://a4study.org/a4-study-team. **The A4 Study is funded by a public-private-philanthropic partnership, including funding from the National Institutes of Health-National Institute on Aging (R01AG063689, U19AG010483, U24AG057437), Eli Lilly and Company, Alzheimer's Association, Accelerating Medicines Partnership through the Foundation for the National Institutes of Health, GHR Foundation, Davis Alzheimer Prevention Program, an anonymous foundation and additional private donors to the Brigham and Women's Hospital, with in-kind support from Avid and Cogstate, Albert Einstein College of Medicine, and the Foundation for Neurologic Disease. The companion observational Longitudinal Evaluation of Amyloid Risk and Neurodegeneration (LEARN) Study is funded by the Alzheimer's Association and GHR Foundation. ***Part of data used in the preparation of this article were obtained from the DELCODE study https://www.dzne.de/en/research/studies/clinicalstudies/delcode/ The authors thank the following institutions: Max-Delbrück#x02010;centrum f#x000FC;r Molekulare medizin in der Helmholtz#x02010;Gemeinschaft (MDC), Freie Universität Berlin Center for Cognitive neuroscience Berlin (CCNB), Klinik und Poliklinik für Nuklearmedizin. Universitätsklinikum Bonn. Venusberg-Campus 1, Uniklinik Köln - Klinik und Poliklinik für Nuklearmedizin, Universitätsklinik Magdeburg-Zentrum für Radiologie Klinik für Radiologie und Nuklearmedizin, Klinik und Poliklinik für Nuklearmedizin Klinikum der Universität München, Universitätsklinikum Rostock Klinik und Poliklinik für Nuklearmedizin, Nuklearmedizin und Klinische Molekulare Bildgebung - Univeristätsklinikum Tübingen, Bernstein Center für Computational Neuroscience Berlin, Universitätsmedizin Göttingen Core Facility MR-Research Göttingen, Institut für Klinische Radiologie Klinikum der Universität München, Universitätsklinikum Tübingen MR-Forschungszentrum. ***The DELCODE study was funded by the German Center for Neurodegenerative Diseases (Deutsches Zentrum für Neurodegenerative Erkrankungen (DZNE)), reference number BN012. ****Part of data used in the preparation of this article were obtained from the Harvard Aging Brain Study, dataset version 2.00 (HABS - P01AG036694; https://habs.mgh.harvard.edu/. The HABS study was launched in 2010, funded by the National Institute on Aging, and is led by principal investigators Reisa A. Sperling MD and Keith A. Johnson MD at Massachusetts General Hospital/Harvard Medical School in Boston, MA. ****The HABS study was funded by the National Institute on Aging P01AG036694. Part of data used in the preparation of this article were obtained from the IMAP+ study (https://neuropresage.fr/imap/). The authors thank the scientific collaborators of the project and the Cyceron MRI-PET staff members for the administrative support and their help with the data acquisition. The authors also thank the patients and healthy volunteers who were included in this study. The Imagerie Multimodale de la maladie d'Alzheimer a un stade Precoce study (IMAP, G Chételat, Caen) was supported by the Programme Hospitalier de Recherche Clinique (PHRCN 2011-A01493-38 and PHRCN 2012 12-006-0347), the Agence Nationale de la Recherche (ANR LONGVIE 2007), Fondation Plan Alzheimer (Alzheimer Plan 20082012), Association France Alzheimer et maladies apparentées (AAP 2013), the Région Basse Normandie and the Institut National de la Santé et de la Recherche Médicale (INSERM). Part of data used in the preparation of this article were obtained from the SCIENCe project (https://researchinformation.amsterdamumc.org/en/) Research of Alzheimer Centre Amsterdam is part of the neurodegeneration research program of Amsterdam Neuroscience. Alzheimer Centre Amsterdam is supported by Stichting Alzheimer Nederland and Stichting Steun Alzheimercentrum Amsterdam. The SCIENCe project is supported by research grants stichting Dioraphte and the Noaber foundation. [18F]florbetapir PET scans were funded by AVID. Wiesje van der Flier holds the Pasman chair. Part of data used in the preparation of this article were obtained from the Vanderbilt Memory and Aging Project (VMAP, Alzheimer's Association IIRG-08-88733, R01-AG034962, https://www.vumc.org/vmac/vmap) VMAP was started in 2012 and is led by Principal Investigator Dr. Angela Jefferson as part of the Vanderbilt Memory and Alzheimer's Center Investigators at Vanderbilt University Medical Center. The authors thank Leslie Gaynor, Timothy Hohman, Angela Jefferson, Elizabeth Moore, VMAP collaborators and staff members, and the participants and their families who participate in this study. The VMAP study is supported by Alzheimer's Association IIRG-08-88733, R01-AG034962 (PI: Jefferson), R01-AG062826, and UL1-TR000445. Part of data used in the preparation of this article were obtained from the Wisconsin Registry for Alzheimer's Prevention (WRAP, https://wrap.wisc.edu). The WRAP study is supported by NIA grant R01-AG027161 (SCJ; Wisconsin Registry for Alzheimer Prevention: Biomarkers of Preclinical AD). WRAP is also supported by the Clinical and Translational Science Award (CTSA) program, through the NIH National Center for Advancing Translational Sciences (NCATS), grant UL1TR000427. **Part of data used in the preparation of this article were obtained from the A4 Study ( https://a4study.org/ ) is a secondary prevention trial in preclinical Alzheimer's disease, aiming to slow cognitive decline associated with brain amyloid accumulation in clinically normal older individuals. The A4 and LEARN Studies are led by Dr. Reisa Sperling at Brigham and Women's Hospital, Harvard Medical School and Dr. Paul Aisen at the Alzheimer's Therapeutic Research Institute (ATRI), University of Southern California. The A4 and LEARN Studies are coordinated by ATRI at the University of Southern California, and the data are made available through the Laboratory for Neuro Imaging at the University of Southern California. The participants screening for the A4 Study provided permission to share their de‐identified data in order to advance the quest to find a successful treatment for Alzheimer's disease. We would like to acknowledge the dedication of all the participants, the site personnel, and all of the partnership team members who continue to make the A4 and LEARN Studies possible. The complete A4 Study Team list is available on: http://a4study.org/a4-study-team . **The A4 Study is funded by a public‐private‐philanthropic partnership, including funding from the National Institutes of Health‐National Institute on Aging (R01AG063689, U19AG010483, U24AG057437), Eli Lilly and Company, Alzheimer's Association, Accelerating Medicines Partnership through the Foundation for the National Institutes of Health, GHR Foundation, Davis Alzheimer Prevention Program, an anonymous foundation and additional private donors to the Brigham and Women's Hospital, with in‐kind support from Avid and Cogstate, Albert Einstein College of Medicine, and the Foundation for Neurologic Disease. The companion observational Longitudinal Evaluation of Amyloid Risk and Neurodegeneration (LEARN) Study is funded by the Alzheimer's Association and GHR Foundation. ***Part of data used in the preparation of this article were obtained from the DELCODE study https://www.dzne.de/en/research/studies/clinicalstudies/delcode/ The authors thank the following institutions: Max‐Delbrück#x02010;centrum f#x000FC;r Molekulare medizin in der Helmholtz#x02010;Gemeinschaft (MDC), Freie Universität Berlin Center for Cognitive neuroscience Berlin (CCNB), Klinik und Poliklinik für Nuklearmedizin. Universitätsklinikum Bonn. Venusberg‐Campus 1, Uniklinik Köln ‐ Klinik und Poliklinik für Nuklearmedizin, Universitätsklinik Magdeburg‐Zentrum für Radiologie Klinik für Radiologie und Nuklearmedizin, Klinik und Poliklinik für Nuklearmedizin Klinikum der Universität München, Universitätsklinikum Rostock Klinik und Poliklinik für Nuklearmedizin, Nuklearmedizin und Klinische Molekulare Bildgebung ‐ Univeristätsklinikum Tübingen, Bernstein Center für Computational Neuroscience Berlin, Universitätsmedizin Göttingen Core Facility MR‐Research Göttingen, Institut für Klinische Radiologie Klinikum der Universität München, Universitätsklinikum Tübingen MR‐Forschungszentrum. ***The DELCODE study was funded by the German Center for Neurodegenerative Diseases (Deutsches Zentrum für Neurodegenerative Erkrankungen (DZNE)), reference number BN012. Part of data used in the preparation of this article were obtained from the SCIENCe project ( https://researchinformation.amsterdamumc.org/en/ ) Research of Alzheimer Centre Amsterdam is part of the neurodegeneration research program of Amsterdam Neuroscience. Alzheimer Centre Amsterdam is supported by Stichting Alzheimer Nederland and Stichting Steun Alzheimercentrum Amsterdam. The SCIENCe project is supported by research grants stichting Dioraphte and the Noaber foundation. [F]florbetapir PET scans were funded by AVID. Wiesje van der Flier holds the Pasman chair. Elizabeth Kuhn was funded by the University of Caen Normandy, INSERM, the Fondation Philippe Chatrier and the Helmholtz Association's Initiative and Networking Fund through Helmholtz Artificial Intelligence Cooperation Unit (ZT‐I‐PF‐5‐163). Rachel Buckley is funded by a NIH Pathway to Independence award, R00‐AG061238, an NIH New Innovator award, DP2AG082342, and an R01‐AG079142. Katherine A. Gifford was funded by a K23‐AG045966 and R01‐AG062826. Gonzalo Sánchez Benavides is supported by Instituto de Salud Carlos III (ISCIII) through the project CP23/00039 (Miguel Servet contract), co‐funded by the European Union (FSE+). *Part of the data used in preparation of this article was obtained from the Alzheimer's Disease Neuroimaging Initiative (ADNI) database ( https://adni.loni.usc.edu ) As such, the investigators within the ADNI contributed to the design and implementation of ADNI and/or provided data, but they did not participate in analysis or writing of this report. A complete listing of ADNI investigators can be found at: http://adni.loni.usc.edu/wpcontent/uploads/how_to_apply/ADNI_Acknowledgement_List.pdf . The ADNI was launched in 2003 as a public‐private partnership led by Principal Investigator Michael W. Weiner, MD. The primary goal of ADNI has been to test whether serial magnetic resonance imaging (MRI), positron emission tomography (PET), other biological markers, and clinical and neuropsychological assessment can be combined to measure the progression of mild cognitive impairment (MCI) and early Alzheimer's disease (AD). *ADNI data collection and sharing for this project was funded by the ADNI (National Institutes of Health Grant U01 AG024904) and DOD ADNI (Department of Defense award number W81XWH‐12‐2‐0012). ADNI is funded by the National Institute on Aging, the National Institute of Biomedical Imaging and Bioengineering, and through generous contributions from the following: AbbVie, Alzheimer's Association; Alzheimer's Drug Discovery Foundation; Araclon Biotech; BioClinica, Inc.; Biogen; Bristol‐Myers Squibb Company; CereSpir, Inc.; Cogstate; Eisai Inc.; Elan Pharmaceuticals, Inc.; Eli Lilly and Company; EuroImmun; F. Hoffmann‐La Roche Ltd and its affiliated company Genentech, Inc.; Fujirebio; GE Healthcare; IXICO Ltd.; Janssen Alzheimer Immunotherapy Research & Development, LLC.; Johnson & Johnson Pharmaceutical Research & Development LLC.; Lumosity; Lundbeck; Merck & Co., Inc.; Meso Scale Diagnostics, LLC.; NeuroRx Research; Neurotrack Technologies; Novartis Pharmaceuticals Corporation; Pfizer Inc.; Piramal Imaging; Servier; Takeda Pharmaceutical Company; and Transition Therapeutics. The Canadian Institutes of Health Research is providing funds to support ADNI clinical sites in Canada. Private sector contributions are facilitated by the Foundation for the National Institutes of Health ( www.fnih.org ). The grantee organization is the Northern California Institute for Research and Education, and the study is coordinated by the Alzheimer's Therapeutic Research Institute at the University of Southern California. ADNI data are disseminated by the Laboratory for Neuro Imaging at the University of Southern California. Research programs of Wiesje van der Flier (WF) have been funded by ZonMW, NWO, EU‐JPND, EU‐IHI, Alzheimer Nederland, Hersenstichting CardioVascular Onderzoek Nederland, Health∼Holland, Topsector Life Sciences & Health, stichting Dioraphte, Gieskes‐Strijbis fonds, stichting Equilibrio, Edwin Bouw fonds, Pasman stichting, stichting Alzheimer & Neuropsychiatrie Foundation, Philips, Biogen MA Inc, Novartis‐NL, Life‐MI, AVID, Roche BV, Fujifilm, Eisai, and Combinostics. W.F. holds the Pasman chair. W.F. is recipient of ABOARD, which is a public–private partnership receiving funding from ZonMW (#73305095007) and Health∼Holland, Topsector Life Sciences & Health (PPP‐allowance; #LSHM20106). W.F. has been an invited speaker at Biogen MA Inc, Danone, Eisai, WebMD Neurology (Medscape), NovoNordisk, Springer Healthcare, and European Brain Council. W.F. is consultant to Oxford Health Policy Forum CIC, Roche, Biogen MA Inc, and Eisai. W.F. is member of steering cie of NovoNordisk evoke/evoke+. W.F. participated in advisory boards of Biogen MA Inc, Roche, and Eli Lilly; all funding is paid to her institution. W.F. is member of the steering committee of PAVE and Think Brain Health. W.F. was associate editor of in 2020/2021. WF is associate editor at . The authors declare no other relevant competing interests. Author disclosures are available in the supporting information . Alzheimer, Research & Therapy Brain Part of data used in the preparation of this article were obtained from the IMAP+ study ( https://neuropresage.fr/imap/ ). The authors thank the scientific collaborators of the project and the Cyceron MRI‐PET staff members for the administrative support and their help with the data acquisition. The authors also thank the patients and healthy volunteers who were included in this study. The Imagerie Multimodale de la maladie d'Alzheimer a un stade Precoce study (IMAP, G Chételat, Caen) was supported by the Programme Hospitalier de Recherche Clinique (PHRCN 2011‐A01493‐38 and PHRCN 2012 12‐006‐0347), the Agence Nationale de la Recherche (ANR LONGVIE 2007), Fondation Plan Alzheimer (Alzheimer Plan 20082012), Association France Alzheimer et maladies apparentées (AAP 2013), the Région Basse Normandie and the Institut National de la Santé et de la Recherche Médicale (INSERM). Part of data used in the preparation of this article were obtained from the Wisconsin Registry for Alzheimer's Prevention (WRAP, https://wrap.wisc.edu ). The WRAP study is supported by NIA grant R01‐AG027161 (SCJ; Wisconsin Registry for Alzheimer Prevention: Biomarkers of Preclinical AD). WRAP is also supported by the Clinical and Translational Science Award (CTSA) program, through the NIH National Center for Advancing Translational Sciences (NCATS), grant UL1TR000427. Part of data used in the preparation of this article were obtained from the Vanderbilt Memory and Aging Project (VMAP, Alzheimer's Association IIRG‐08‐88733, R01‐AG034962, https://www.vumc.org/vmac/vmap ) VMAP was started in 2012 and is led by Principal Investigator Dr. Angela Jefferson as part of the Vanderbilt Memory and Alzheimer's Center Investigators at Vanderbilt University Medical Center. The authors thank Leslie Gaynor, Timothy Hohman, Angela Jefferson, Elizabeth Moore, VMAP collaborators and staff members, and the participants and their families who participate in this study. The VMAP study is supported by Alzheimer's Association IIRG‐08‐88733, R01‐AG034962 (PI: Jefferson), R01‐AG062826, and UL1‐TR000445. ****Part of data used in the preparation of this article were obtained from the Harvard Aging Brain Study, dataset version 2.00 (HABS ‐ P01AG036694; https://habs.mgh.harvard.edu/ . The HABS study was launched in 2010, funded by the National Institute on Aging, and is led by principal investigators Reisa A. Sperling MD and Keith A. Johnson MD at Massachusetts General Hospital/Harvard Medical School in Boston, MA. ****The HABS study was funded by the National Institute on Aging P01AG036694.

FundersFunder number
Agence Nationale de la Recherche
Northern California Institute for Research and Education
Eli Lilly and Company
Alzheimer's AssociationUL1‐TR000445, IIRG‐08‐88733, R01‐AG062826
Uniklinik Köln - Klinik und Poliklinik für Nuklearmedizin
Alzheimer's Disease Neuroimaging Initiative
Deutsches Zentrum für Neurodegenerative Erkrankungen
Universitätsklinik Magdeburg-Zentrum für Radiologie Klinik für Radiologie und Nuklearmedizin, Klinik und Poliklinik für Nuklearmedizin Klinikum der Universität München, Universitätsklinikum Rostock Klinik und Poliklinik für Nuklearmedizin, Nuklearmedizin und Klinische Molekulare Bildgebung - Univeristätsklinikum Tübingen
Universitätsmedizin Göttingen
Stichting Steun Alzheimercentrum Amsterdam
Fondation Plan Alzheimer20082012
Initiative and Networking Fund
Helmholtz Association
Alzheimer's disease
University of Southern California
Fondation Philippe Chatrier
Klinik und Poliklinik für Nuklearmedizin
Austin Health
Institut national de la santé et de la recherche médicale
Stichting Alzheimer Nederland
National Institute of Biomedical Imaging and Bioengineering
Roche
Alzheimer's Drug Discovery Foundation
Alzheimer Nederland
Wisconsin Registry for Alzheimer's Prevention
University of Melbourne
Harvard Medical School
CCNB
European Commission
European Social Fund Plus
Freie Universität Berlin Center for Cognitive neuroscience Berlin
Edith Cowan University
ADNI
Noaber FoundationR01-AG034962
ANR
NIH National Center for Advancing Translational Sciences
Commonwealth Scientific and Industrial Research Organisation
Bernstein Center für Computational Neuroscience Berlin
Foundation for Neurologic Diseases
Région Basse Normandie
Department of Defense
Foundation for Neurologic Disease
Universitätsklinikum Tübingen
GHR Foundation
German Center for Neurodegenerative Diseases
Biogen
ISTAART
Araclon Biotech
NWO
DOD ADNI
AbbVie
National Ageing Research Institute
ZonMw
BioClinica, Inc.
Université de Caen Normandie
Association de soutien à la Paralysie Supranucléaire Progressive
National Institutes of Health‐National Institute on AgingU19AG010483, U24AG057437, R01AG063689
National Institutes of HealthU01 AG024904, R01-AG079142, R00‐AG061238, K23-AG045966, R01‐AG062826, DP2AG082342
Harvard Aging Brain StudyHABS - P01AG036694
DZNEBN012
AssociationAAP 2013
U.S. Department of DefenseW81XWH‐12‐2‐0012
Programme Hospitalier de Recherche CliniquePHRCN 2012 12‐006‐0347
National Center for Advancing Translational SciencesUL1TR000427
National Institute on AgingP01AG036694, U19AG010483, U24AG057437, R01AG063689, R01-AG027161
NIAR01‐AG027161
NCATSUL1TR000427
Instituto de Salud Carlos IIICP23/00039
Helmholtz Artificial Intelligence Cooperation UnitZT‐I‐PF‐5‐163

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