P‐tau217 significance as marker of brain Abeta and tau pathologies

P-tau217 is a highly accurate marker of Abeta deposition. The strong association between p-tau217 and Abeta PET, when tau PET remains negative, supports tau hyperphosphorylation is a neuronal response to Abeta pathology independent from tau aggregation. On the other hand, p-tau217 associates with tau-PET at prodromal AD stage and occasionally changes in participants with primary tauopathies free of amyloid deposition. This corroborates soluble p-tau217 also increases because of the presence of brain tau aggregates. The duality of p-tau217 response to amyloid and tau pathology in AD complicates its utility as marker of tau aggregation. Lastly, plasma p-tau217 use as a single marker of Abeta positivity may expose to risk of false positive AD diagnosis for patients with primary tauopathies.

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Publication Details

Journal
Alzheimer s & Dementia
Published
2024-12-01
DOI
https://doi.org/10.1002/alz.089427
Primary Topic
Alzheimer's disease research and treatments
Type
article
Field-Weighted Citation Impact
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article

P‐tau217 significance as marker of brain Abeta and tau pathologies

Tammie L.S. Benzinger, Lawren VandeVrede, Richard J. Perrin, Adam L. Boxer et al.
Alzheimer s & Dementia
Alzheimer's disease research and treatments
article

P‐tau217 significance as marker of brain Abeta and tau pathologies

Tammie L.S. Benzinger, Lawren VandeVrede, Richard J. Perrin, Adam L. Boxer, Audrey Gabelle, Randall John Bateman, Chihiro Sato, Salvatore Spina, Yingxin He, Oskar Hansson, Gemma Salvadó, Eric McDade, Nicolas R. Barthélemy, Ross W. Paterson, Suzanne E. Schindler, Nupur Ghoshal, Kanta Horie, Brian A. Gordon, Yan Li, Soumya Mukherjee, Shorena Janelidze
article en

Abstract

P-tau217 is a highly accurate marker of Abeta deposition. The strong association between p-tau217 and Abeta PET, when tau PET remains negative, supports tau hyperphosphorylation is a neuronal response to Abeta pathology independent from tau aggregation. On the other hand, p-tau217 associates with tau-PET at prodromal AD stage and occasionally changes in participants with primary tauopathies free of amyloid deposition. This corroborates soluble p-tau217 also increases because of the presence of brain tau aggregates. The duality of p-tau217 response to amyloid and tau pathology in AD complicates its utility as marker of tau aggregation. Lastly, plasma p-tau217 use as a single marker of Abeta positivity may expose to risk of false positive AD diagnosis for patients with primary tauopathies.

Alzheimer s & DementiaVol. 20(S1)
University of California, San Francisco (US), Lund University (SE), Washington University in St. Louis (US), National Hospital for Neurology and Neurosurgery (GB), University College London (GB)
Openalex Percentile: Top 66%
Alzheimer's disease research and treatments
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