Towards clinical application of tau PET tracers for diagnosing dementia due to Alzheimer's disease

2021 ◽  
Author(s):  
Rik Ossenkoppele ◽  
Oskar Hansson
2020 ◽  
Vol 16 (S5) ◽  
Author(s):  
Gerard N. Bischof ◽  
Alessandra Dodich ◽  
Nicholas J Ashton ◽  
Marina Boccardi ◽  
Henryk Barthel ◽  
...  

2021 ◽  
Vol 93 ◽  
pp. 11-18
Author(s):  
Pradith Lerdsirisuk ◽  
Ryuichi Harada ◽  
Yoshimi Hayakawa ◽  
Yuki Shimizu ◽  
Yoichi Ishikawa ◽  
...  

Author(s):  
Gérard N Bischof ◽  
Alessandra Dodich ◽  
Marina Boccardi ◽  
Thilo van Eimeren ◽  
Cristina Festari ◽  
...  

Abstract Purpose In 2017, the Geneva Alzheimer’s disease (AD) strategic biomarker roadmap initiative proposed a framework of the systematic validation AD biomarkers to harmonize and accelerate their development and implementation in clinical practice. Here, we use this framework to examine the translatability of the second-generation tau PET tracers into the clinical context. Methods All available literature was systematically searched based on a set of search terms that related independently to analytic validity (phases 1–2), clinical validity (phase 3–4), and clinical utility (phase 5). The progress on each of the phases was determined based on scientific criteria applied for each phase and coded as fully, partially, preliminary achieved or not achieved at all. Results The validation of the second-generation tau PET tracers has successfully passed the analytical phase 1 of the strategic biomarker roadmap. Assay definition studies showed evidence on the superiority over first-generation tau PET tracers in terms of off-target binding. Studies have partially achieved the primary aim of the analytical validity stage (phase 2), and preliminary evidence has been provided for the assessment of covariates on PET signal retention. Studies investigating of the clinical validity in phases 3, 4, and 5 are still underway. Conclusion The current literature provides overall preliminary evidence on the establishment of the second-generation tau PET tracers into the clinical context, thereby successfully addressing some methodological issues from the tau PET tracer of the first generation. Nevertheless, bigger cohort studies, longitudinal follow-up, and examination of diverse disease population are still needed to gauge their clinical validity.


Brain ◽  
2016 ◽  
Vol 139 (5) ◽  
pp. 1551-1567 ◽  
Author(s):  
Rik Ossenkoppele ◽  
Daniel R. Schonhaut ◽  
Michael Schöll ◽  
Samuel N. Lockhart ◽  
Nagehan Ayakta ◽  
...  

2017 ◽  
Vol 23 (7) ◽  
pp. 1666-1673 ◽  
Author(s):  
K Chiotis ◽  
L Saint-Aubert ◽  
E Rodriguez-Vieitez ◽  
A Leuzy ◽  
O Almkvist ◽  
...  

2021 ◽  
Author(s):  
Niklas Mattsson-Carlgren ◽  
Shorena Janelidze ◽  
Randall Bateman ◽  
Ruben Smith ◽  
Erik Stomrud ◽  
...  

Abstract Alzheimer’s disease is characterized by β-amyloid plaques and tau tangles. Plasma levels of phospho-tau217 (P-tau217) accurately differentiate Alzheimer’s disease dementia from other dementias, but it is unclear to what degree this reflects β-amyloid plaque accumulation, tau tangle accumulation, or both. In a cohort with post-mortem neuropathological data (N=88), both plaque and tangle density contributed independently to higher P-tau217. Several findings were replicated in a cohort with PET imaging (“BioFINDER-2”, N=426), where β-amyloid and tau PET were independently associated to P-tau217. P-tau217 correlated with β-amyloid PET (but not tau PET) in early disease stages, and with both β-amyloid and (more strongly) tau PET in late disease stages. Finally, P-tau217 mediated the association between β-amyloid and tau in both cohorts, especially for tau outside of the medial temporal lobe. These findings support the hypothesis that plasma P-tau217 is increased by both β-amyloid plaques and tau tangles and is congruent with the hypothesis that P-tau is involved in β-amyloid-dependent formation of neocortical tau tangles.


Sign in / Sign up

Export Citation Format

Share Document