HAI Book 2025 - Flipbook - Page 677
Trudel, Lydia
165
Patterns of tau-PET accumulation and clinical progression
according to biological AD stages
Lydia Trudel1,2, Joseph Therriault1, Nesrine Rahmouni1,2, Arthur Cassa Macedo1,2, Stijn
Servaes1,2, Etienne Aumont1, Seyyed Ali Hosseini1,2, Jaime Fernandez-Arias1,2, Yansheng
Zheng1,2, Yi-Ting Wang1,2, Tevy Chan1,2, Brandon Hall1,2, Jenna Stevenson1, Robert Hopewell4,
Chris Hung-Hsin Hsiao4, Serge Gauthier1, Paolo Vitali1, Tharick Pascoal3, Pedro Rosa-Neto1,2
1
Translational Neuroimaging Laboratory, McGill University, Montreal, QC, CA
Department of Neurology and Neurosurgery, Faculty of Medicine, McGill University, Montreal, QC, CA
3
Department of Psychiatry, School of Medicine, University of Pittsburgh, Pittsburgh, PA, US
4
PET Unit, McConnell Brain Imaging Centre, Montreal, QC, CA
2
Objectives: Recently, the Alzheimer9s Association Workgroup proposed a framework in which tau-PET can stage
AD severity in vivo. In this framework, AD severity is staged as T2-, T2MTL+, T2MOD+ and T2HIGH+ based on tau-PET
patterns. The goal of this study is to identify stage-specific patterns of tau-PET accumulation, as well as describe
rates of clinical and biological AD stage progression.
Methods: We analyzed tau-PET imaging data from 545 individuals from the TRIAD and ADNI cohorts followed over
an average of 3.49 years. Amyloid-positive participants were staged based on regional tau-PET uptake and
amyloid-negative individuals were included as non-AD controls. We assessed stage-specific tau accumulation in
early, intermediate and late ROIs. Rates of biological AD stage progression were identified for one-year and twoyear follow-up. Finally, we assessed probability of developing MCI or dementia according to biological AD stage at
baseline using Kaplan-Meier survival analyses.
Results: Individuals showed stage-specific patterns of tau accumulation, predominantly in regions corresponding
to their current stage and the subsequent stage. Notably, those in advanced stages did not exhibit accumulation
in earlier regions (Fig. 1). After two years, we observed low rates of biological stage progression in the T2- group
and substantially higher rates of biological stage progression in T2MTL+ (31.03%) and T2MOD+ groups (42.11%) (Fig. 2).
Survival analyses revealed differential risk of clinical progression according to biological AD stage, with T2MTL+ and
T2MOD+ groups having increased risk of developing MCI, and the T2HIGH+ group of developing dementia over 7 years
(p
