The impact of demographic, clinical, genetic, and imaging variables on tau PET status
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ORIGINAL ARTICLE
The impact of demographic, clinical, genetic, and imaging variables on tau PET status Rik Ossenkoppele 1,2 & Antoine Leuzy 1 & Hanna Cho 3 & Carole H. Sudre 4,5,6 & Olof Strandberg 1 & Ruben Smith 1 & Sebastian Palmqvist 1 & Niklas Mattsson-Carlgren 1,7,8 & Tomas Olsson 9 & Jonas Jögi 10 & Erik Stormrud 1,11 & Young Hoon Ryu 12 & Jae Yong Choi 12,13 & for the Alzheimer’s Disease Neuroimaging Initiative & for the PREVENT-AD research group & Adam L. Boxer 14 & Maria L. Gorno-Tempini 14 & Bruce L. Miller 14 & David Soleimani-Meigooni 14 & Leonardo Iaccarino 14 & Renaud La Joie 14 & Edilio Borroni 15 & Gregory Klein 15 & Michael J. Pontecorvo 16 & Michael D. Devous Sr 16 & Sylvia Villeneuve 17 & Chul Hyoung Lyoo 3 & Gil D. Rabinovici 15,18,19 & Oskar Hansson 1,11 Received: 24 September 2020 / Accepted: 27 October 2020 # The Author(s) 2020
Abstract Purpose A substantial proportion of amyloid-β (Aβ)+ patients with clinically diagnosed Alzheimer’s disease (AD) dementia and mild cognitive impairment (MCI) are tau PET–negative, while some clinically diagnosed non-AD neurodegenerative disorder (non-AD) patients or cognitively unimpaired (CU) subjects are tau PET–positive. We investigated which demographic, clinical, genetic, and imaging variables contributed to tau PET status. Methods We included 2338 participants (430 Aβ+ AD dementia, 381 Aβ+ MCI, 370 non-AD, and 1157 CU) who underwent [18F]flortaucipir (n = 1944) or [18F]RO948 (n = 719) PET. Tau PET positivity was determined in the entorhinal cortex, temporal meta-ROI, and Braak V-VI regions using previously established cutoffs. We performed bivariate binary logistic regression models with tau PET status (positive/negative) as dependent variable and age, sex, APOEε4, Aβ status (only in CU and nonAD analyses), MMSE, global white matter hyperintensities (WMH), and AD-signature cortical thickness as predictors. Additionally, we performed multivariable binary logistic regression models to account for all other predictors in the same model. Results Tau PET positivity in the temporal meta-ROI was 88.6% for AD dementia, 46.5% for MCI, 9.5% for non-AD, and 6.1% for CU. Among Aβ+ participants with AD dementia and MCI, lower age, MMSE score, and AD-signature cortical thickness showed the strongest associations with tau PET positivity. In non-AD and CU participants, presence of Aβ was the strongest predictor of a positive tau PET scan.
Data used in preparation of this article were obtained from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) database (adni.loni.usc.edu). As such, the investigators within the ADNI contributed to the design and implementation of ADNI and/or provided data but 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 Data used in preparation of this article were obtained from the Presymptomatic Evaluation of Novel or Experimental Treatments for Alzheimer’s Disease (PREVENT-AD) program
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