Abstract
Original language | English |
---|---|
Journal | Alzheimer's and Dementia |
Early online date | 2022 |
DOIs | |
Publication status | E-pub ahead of print - 2022 |
Keywords
- AD
- PET
- blood biomarkers
- cognition
- tau
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In: Alzheimer's and Dementia, 2022.
Research output: Contribution to journal › Article › Academic › peer-review
TY - JOUR
T1 - Tau-PET is superior to phospho-tau when predicting cognitive decline in symptomatic AD patients
AU - Smith, Ruben
AU - Cullen, Nicholas C.
AU - Pichet Binette, Alexa
AU - Leuzy, Antoine
AU - Blennow, Kaj
AU - Zetterberg, Henrik
AU - Klein, Gregory
AU - Borroni, Edilio
AU - Ossenkoppele, Rik
AU - Janelidze, Shorena
AU - Palmqvist, Sebastian
AU - Alzheimer's Disease Neuroimaging Initiative
AU - Mattsson-Carlgren, Niklas
AU - Stomrud, Erik
AU - Hansson, Oskar
N1 - Funding Information: The authors wish to thank the participants of the study. The precursor of [18F]RO948 was kindly provided by Hoffman La Roche. Work at the authors’ research center was supported by the Swedish Research Council (2016‐00906), the Knut and Alice Wallenberg Foundation (2017‐0383), the Marianne and Marcus Wallenberg Foundation (2015.0125), the Strategic Research Area MultiPark (Multidisciplinary Research in Parkinson's disease) at Lund University, the Swedish Alzheimer Foundation (AF‐939932; AF‐939981), the Swedish Brain Foundation (FO2019‐0326), the Parkinson Foundation of Sweden (1280/20), the Skåne University Hospital Foundation (2020‐O000028), Regionalt Forskningsstöd (2020‐0314), and the Swedish Federal Government under the ALF agreement (2018‐Projekt0279). H.Z. is a Wallenberg Scholar supported by grants from the Swedish Research Council (#2018‐02532); the European Research Council (#681712); Swedish State Support for Clinical Research (#ALFGBG‐720931); the Alzheimer's 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 Olav Thon Foundation; the Erling‐Persson Family Foundation, Stiftelsen för Gamla Tjänarinnor, Hjärnfonden, Sweden (#FO2019‐0228); the European Union's Horizon 2020 research and innovation programme under the Marie Skłodowska‐Curie grant agreement no. 860197 (MIRIADE); and the UK Dementia Research Institute at UCL. K.B. is supported by the Swedish Research Council (#2017‐00915); the Alzheimer's Drug Discovery Foundation (ADDF), USA (#RDAPB‐201809‐2016615); the Swedish Alzheimer Foundation (#AF‐742881), Hjärnfonden, Sweden (#FO2017‐0243); the Swedish state under the agreement between the Swedish Government and the County Councils; the ALF‐agreement (#ALFGBG‐715986); the European Union Joint Program for Neurodegenerative Disorders (JPND2019‐466‐236); and the National Institutes of Health (NIH), USA (grant #1R01AG068398‐01). ADNI funding: Data collection and sharing for this project was funded by the Alzheimer's Disease Neuroimaging Initiative (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. 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. Publisher Copyright: © 2022 The Authors. Alzheimer's & Dementia published by Wiley Periodicals LLC on behalf of Alzheimer's Association.
PY - 2022
Y1 - 2022
N2 - Introduction: Biomarkers for the prediction of cognitive decline in patients with amnestic mild cognitive impairment (MCI) and amnestic mild dementia are needed for both clinical practice and clinical trials. Methods: We evaluated the ability of tau-PET (positron emission tomography), cortical atrophy on magnetic resonance imaging (MRI), baseline cognition, apolipoprotein E gene (APOE) status, plasma and cerebrospinal fluid (CSF) levels of phosphorylated tau-217, neurofilament light (NfL), and amyloid beta (Aβ)42/40 ratio (individually and in combination) to predict cognitive decline over 2 years in BioFINDER-2 and Alzheimer's Disease Neuroimaging Initiative (ADNI). Results: Baseline tau-PET and a composite baseline cognitive score were the strongest independent predictors of cognitive decline. Cortical thickness and NfL provided some additional information. Using a predictive algorithm to enrich patient selection in a theoretical clinical trial led to a significantly lower required sample size. Discussion: Models including baseline tau-PET and cognition consistently provided the best prediction of change in cognitive function over 2 years in patients with amnestic MCI or mild dementia.
AB - Introduction: Biomarkers for the prediction of cognitive decline in patients with amnestic mild cognitive impairment (MCI) and amnestic mild dementia are needed for both clinical practice and clinical trials. Methods: We evaluated the ability of tau-PET (positron emission tomography), cortical atrophy on magnetic resonance imaging (MRI), baseline cognition, apolipoprotein E gene (APOE) status, plasma and cerebrospinal fluid (CSF) levels of phosphorylated tau-217, neurofilament light (NfL), and amyloid beta (Aβ)42/40 ratio (individually and in combination) to predict cognitive decline over 2 years in BioFINDER-2 and Alzheimer's Disease Neuroimaging Initiative (ADNI). Results: Baseline tau-PET and a composite baseline cognitive score were the strongest independent predictors of cognitive decline. Cortical thickness and NfL provided some additional information. Using a predictive algorithm to enrich patient selection in a theoretical clinical trial led to a significantly lower required sample size. Discussion: Models including baseline tau-PET and cognition consistently provided the best prediction of change in cognitive function over 2 years in patients with amnestic MCI or mild dementia.
KW - AD
KW - PET
KW - blood biomarkers
KW - cognition
KW - tau
UR - http://www.scopus.com/inward/record.url?scp=85144164556&partnerID=8YFLogxK
U2 - https://doi.org/10.1002/alz.12875
DO - https://doi.org/10.1002/alz.12875
M3 - Article
C2 - 36516028
SN - 1552-5260
JO - Alzheimer's and Dementia
JF - Alzheimer's and Dementia
ER -