Plasma biomarker progression across the Alzheimer's disease amyloid beta and tau positron emission tomography trajectories
Year: 2026
Type: article
Study design: Observational Study
Abstract: INTRODUCTION: With increased uptake in disease-modifying treatments for amyloid beta (Aβ) removal, it is important to measure performance of highly sensitive plasma biomarkers to detect the presence of Aβ and tau in cognitively impaired populations. METHODS: In this study, we investigated a large set of plasma biomarkers for their capability to predict Aβ and tau positron emission tomography (PET) and their association with increasing Aβ and tau burden. RESULTS: From the biomarkers assessed, tau phosphorylated at threonine 217 (pTau217) showed the largest increases across the full range of Aβ and tau levels. Furthermore, pTau217/Aβ42 had the smallest proportion of participants in the intermediate zone (∼4%) to predict Aβ status using a 90/90% dual cut-off for sensitivity and specificity, with < 20% of participants in the intermediate zone using the 95/95% dual cut-off. DISCUSSION: While the studied biomarkers proved their utility to predict Aβ and tau PET at their respective thresholds, each has separate quantified responses to Aβ and tau aggregation.
Source: Alzheimer s & Dementia
DOI: 10.1002/alz.71145
Authors: Rodrigo Cánovas, Christopher J. Fowler, Azadeh Feizpour, Vincent Dóre, Pierrick Bourgeat, Ziad S. Saad, Gallen Triana‐Baltzer, Hartmuth C. Kolb, Manu Vandijck, Gwendlyn Kollmorgen, Clara Quijano‐Rubio, Jurgen Fripp, Simon Laws, Anthony W. Bannon, Kaj Blennow, Henrik Zetterberg, Stephanie Rainey‐Smith, Sulantha Mathotaarachchi, Christopher C. Rowe, Colin L. Masters, James D. Doecke
Institutions: Commonwealth Scientific and Industrial Research Organisation, Australian e-Health Research Centre, The University of Melbourne, Florey Institute of Neuroscience and Mental Health, Austin Health, Johnson & Johnson (United States), Fujirebio (Belgium), Roche (Switzerland), Roche Diagnostics International AG (Switzerland), Edith Cowan University, Curtin University, AbbVie (United States), University of Gothenburg, University of Wisconsin–Madison, Sahlgrenska University Hospital, National Hospital for Neurology and Neurosurgery, UCL Queen Square Institute of Neurology, University College London, Murdoch University, The University of Western Australia, Australian Alzheimer’s Research Foundation
Language: English
Subfield: Psychiatry and Mental health
Field: Medicine
Domain: Health Sciences
Open Access status: hybrid
Estimated APC paid: $4,200
Funders: Alzheimer's Association, Alzheimer's Drug Discovery Foundation, Roche, Biogen, AbbVie, Familjen Erling-Perssons Stiftelse, Cure Alzheimer's Fund, Stiftelsen för Gamla Tjänarinnor, EU Joint Programme – Neurodegenerative Disease Research, National Institute for Health and Care Research, University College London, European Commission, Eisai, Hjärnfonden, Vetenskapsrådet, UK Dementia Research Institute, Johnson and Johnson, HORIZON EUROPE Framework Programme, National Health and Medical Research Council
Awards: G1057200632, G1088883541, G150733400, G1551449788, G1588116593, G1771944843, G1802301745, G1833008592, G201353144, G2057385626, G237833635, G2543812357, G2799940023, G292763017, G3241251457, Fluid biomarkers for neurodegenerative dementias, G3903502641, G3914690605, G4234328627, G4260843567, G432431387, G434337789, G4377393254, G5040492720, G506008078, G516766298, Fluid biomarkers for neurodegenerative dementias, CASCADE: CAuSe or Consequence in Alzheimer DiseasE?, G6158734006, G6289970089, Multi-omics Interdisciplinary Research Integration to Address DEmentia diagnosis, G6745400708, G691317373
OpenAlex ID: W7128549290