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Neurology ◽  
2022 ◽  
pp. 10.1212/WNL.0000000000013299
Author(s):  
Pontus Tideman ◽  
Erik Stomrud ◽  
Antoine Leuzy ◽  
Niklas Mattsson-Carlgren ◽  
Sebastian Palmqvist ◽  
...  

Background and Objectives:The neuropathological changes underlying Alzheimer´s disease (AD) start before overt cognitive symptoms arise, but it is not well-known how they relate to the first subtle cognitive changes. The objective for this study was to examine the independent associations of the AD hallmarks β-amyloid (Aβ), tau, and neurodegeneration with different cognitive domains in cognitively unimpaired (CU) individuals.Methods:In this cross-sectional study, CU participants from the prospective BioFINDER-2 study were included. All had CSF biomarkers (Aβ42 and P-tau181), MRI (cortical thickness of AD-susceptible regions), Aβ-PET (neocortical uptake), tau-PET (entorhinal uptake), and cognitive test data for i) memory, ii) executive function, iii) verbal function, iv), and visuospatial function. Multivariable linear regression models were performed, using either CSF Aβ42, P-tau181 and cortical thickness or Aβ-PET, tau-PET, and cortical thickness, as predictors of cognitive function. The results were validated in an independent cohort (ADNI).Results:316 CU participants were included from the BioFINDER-2 study. Abnormal Aβ-status was independently associated with the executive measure, regardless of modality (CSF Aβ42 β=0.128, p=0.024; Aβ-PET β=0.124, p=0.049), while tau was independently associated with memory (CSF P-tau181 β=0.132, p=0.018; tau-PET β=0.189, p=0.002). Cortical thickness was independently associated with the executive measure and verbal fluency in both models (p=0.005-0.018). To examine the relationships in the earliest stage of preclinical AD, only participants with normal biomarkers of tau and neurodegeneration were included (n=217 CSF-based; n=246 PET-based). Again, Aβ-status was associated with executive function (CSF Aβ42, β=0.189, p=0.005; Aβ-PET, β=0.146, p=0.023), but not with other cognitive domains. The results were overall replicated in the ADNI cohort (n=361).Discussion:These findings suggest that Aβ is independently associated with worse performance on an executive measure but not with memory performance, which instead is associated with tau pathology. This may have implications for early preclinical AD screening and outcome measures in AD trials targeting Aβ pathology.


2022 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Chenhao Jia ◽  
Meiqi Wu ◽  
Tzu-Chen Yen ◽  
Yanfeng Li ◽  
Ruixue Cui

2021 ◽  
Vol 17 (S5) ◽  
Author(s):  
Rachel F. Buckley ◽  
Adrienne O’Donnell ◽  
Emer R. McGrath ◽  
Heidi I.L. Jacobs ◽  
Claudia L. Satizabal ◽  
...  

2021 ◽  
Vol 17 (S10) ◽  
Author(s):  
Gilda E Ennis ◽  
Tobey J Betthauser ◽  
Rebecca L Koscik ◽  
Corinne D Engelman ◽  
Rozalyn Anderson ◽  
...  

2021 ◽  
Vol 17 (S1) ◽  
Author(s):  
Davina Biel ◽  
Matthias Brendel ◽  
Anna Rubinski ◽  
Katharina Buerger ◽  
Daniel Janowitz ◽  
...  

2021 ◽  
Vol 17 (S9) ◽  
Author(s):  
Guoqiao Wang ◽  
Yan Li ◽  
Chengjie Xiong ◽  
Tammie L.S. Benzinger ◽  
Brian A. Gordon ◽  
...  

2021 ◽  
Vol 17 (S1) ◽  
Author(s):  
James Zou ◽  
David Park ◽  
Aubrey S Johnson ◽  
Zeljko Tomljanovic ◽  
Davangere P. Devanand ◽  
...  

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Edmond Teng ◽  
Paul T. Manser ◽  
Sandra Sanabria Bohorquez ◽  
Kristin R. Wildsmith ◽  
Karen Pickthorn ◽  
...  

Abstract Background The role and implementation of tau PET imaging for predicting subsequent cognitive decline in Alzheimer’s disease (AD) remains uncertain. This study was designed to evaluate the relationship between baseline [18F]GTP1 tau PET and subsequent longitudinal change across multiple cognitive measures over 18 months. Methods Our analyses incorporated data from 67 participants, including cognitively normal controls (n = 10) and β-amyloid (Aβ)-positive individuals ([18F] florbetapir Aβ PET) with prodromal (n = 26), mild (n = 16), or moderate (n = 15) AD. Baseline measurements included cortical volume (MRI), tau burden ([18F]GTP1 tau PET), and cognitive assessments [Mini-Mental State Examination (MMSE), Clinical Dementia Rating (CDR), 13-item version of the Alzheimer’s Disease Assessment Scale-Cognitive Subscale (ADAS-Cog13), and Repeatable Battery for the Assessment of Neuropsychological Status (RBANS)]. Cognitive assessments were repeated at 6-month intervals over an 18-month period. Associations between baseline [18F]GTP1 tau PET indices and longitudinal cognitive performance were assessed via univariate (Spearman correlations) and multivariate (linear mixed effects models) approaches. The utility of potential prognostic tau PET cut points was assessed with ROC curves. Results Univariate analyses indicated that greater baseline [18F]GTP1 tau PET signal was associated with faster rates of subsequent decline on the MMSE, CDR, and ADAS-Cog13 across regions of interest (ROIs). In multivariate analyses adjusted for baseline age, cognitive performance, cortical volume, and Aβ PET SUVR, the prognostic performance of [18F]GTP1 SUVR was most robust in the whole cortical gray ROI. When AD participants were dichotomized into low versus high tau subgroups based on baseline [18F]GTP1 PET standardized uptake value ratios (SUVR) in the temporal (cutoff = 1.325) or whole cortical gray (cutoff = 1.245) ROIs, high tau subgroups demonstrated significantly more decline on the MMSE, CDR, and ADAS-Cog13. Conclusions Our results suggest that [18F]GTP1 tau PET represents a prognostic biomarker in AD and are consistent with data from other tau PET tracers. Tau PET imaging may have utility for identifying AD patients at risk for more rapid cognitive decline and for stratification and/or enrichment of participant selection in AD clinical trials. Trial registration ClinicalTrials.gov NCT02640092. Registered on December 28, 2015


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