24 januari 2024: zie enkele artikelen via deze search met zoekwoord Alzheimer op onze website.

24 januari 2024: Bron: JAMA Neurol. Published online January 22, 2024.

Een eenvoudige bloedtest blijkt tot 96 procent nauwkeurig de ziekte van Alzheimer - dementie te kunnen aantonen door het meten van verhoogde niveaus van beta-amyloid en tot 97 procent bij het identificeren van p-tau217. Deze twee eiwitten veroorzaken de ziekte van Alzheimer - dementie.

De bloedtest kan ook al jaren voordat de ziekte zich manifesteert aantonen dat de ziekte zich gaat voordoen. Verder blijkt de bloedtest een patiëntvriendelijker en goedkoper alternatief voor andere diagnosetechnieken van dementie.  

De ziekte van Alzheimer - dementie is een aandoening die naarmate de ziekte erger wordt iemand steeds meer moeite met dagelijkse vaardigheden krijgt en wordt tot nu toe gezien als ongeneeslijk. Wel kan met vooral een gezonde leefstijl de progressie van de ziekte afgeremd worden, zie enkele artikelen via deze search met zoekwoord Alzheimer op onze website.

Uit een recent gepubliceerde studie bleek dat de p-tau217-immunoassay vergelijkbare nauwkeurigheid vertoonde als biomarkers voor hersenvocht bij het identificeren van abnormale amyloïde β (Aβ) en tau-pathologieën.
In drie verschillende onafhankelijk van elkaar uitgevoerde studies voor het detecteren van abnormale Aβ-pathologie waren de resultaten van de bloedtest consistent in alle drie de studiegroepen;
Over een periode van acht jaar vond de grootste verandering in p-tau217 plaats bij individuen die positief waren voor zowel Aβ als tau.

Het originele studierapport is gratis in te zien. Hier het abstract van deze studie:
January 22, 2024

Diagnostic Accuracy of a Plasma Phosphorylated Tau 217 Immunoassay for Alzheimer Disease Pathology

Nicholas J. Ashton, PhD1,2,3,4; Wagner S. Brum1,5; Guglielmo Di Molfetta, MSc1; et alAndrea L. Benedet, PhD1; Burak Arslan, MD1; Erin Jonaitis, PhD6,7,8; Rebecca E. Langhough, PhD6,7,8; Karly Cody, PhD7; Rachael Wilson, PhD7,8; Cynthia M. Carlsson, PhD6,7,8,9; Eugeen Vanmechelen, PhD10; Laia Montoliu-Gaya, PhD1; Juan Lantero-Rodriguez, PhD1; Nesrine Rahmouni, MSc11,12; Cecile Tissot, PhD11,12; Jenna Stevenson, PhD11,12; Stijn Servaes, PhD11,12; Joseph Therriault, PhD11,12; Tharick Pascoal, MD, PhD13,14; Alberto Lleó, MD, PhD15,16; Daniel Alcolea, MD, PhD15,16; Juan Fortea, MD, PhD15,16; Pedro Rosa-Neto, MD, PhD11,12; Sterling Johnson, MD, PhD6,7; Andreas Jeromin, PhD17; Kaj Blennow, MD, PhD1,18; Henrik Zetterberg, MD, PhD1,7,18,19,20,21
Author Affiliations Article Information
JAMA Neurol. Published online January 22, 2024. doi:10.1001/jamaneurol.2023.5319
Key Points

Question  What are the capabilities of a commercially available plasma phosphorylated tau 217 (p-tau217) immunoassay to identify Alzheimer disease pathophysiology?

Findings  This cohort study found that the p-tau217 immunoassay showed similar accuracies to cerebrospinal fluid biomarkers in identifying abnormal amyloid β (Aβ) and tau pathologies. A 3-range reference for detecting abnormal Aβ pathology was consistent across 3 cohorts; over 8 years, the largest change of p-tau217 was in individuals positive for both Aβ and tau.

Meaning  The wider availability of high-performing assays may expedite the use of blood biomarkers in clinical settings and benefit the research community.

Abstract

Importance  Phosphorylated tau (p-tau) is a specific blood biomarker for Alzheimer disease (AD) pathology, with p-tau217 considered to have the most utility. However, availability of p-tau217 tests for research and clinical use has been limited. Expanding access to this highly accurate AD biomarker is crucial for wider evaluation and implementation of AD blood tests.

Objective  To determine the utility of a novel and commercially available immunoassay for plasma p-tau217 to detect AD pathology and evaluate reference ranges for abnormal amyloid β (Aβ) and longitudinal change across 3 selected cohorts.

Design, Setting, and Participants  This cohort study examined data from 3 single-center observational cohorts: cross-sectional and longitudinal data from the Translational Biomarkers in Aging and Dementia (TRIAD) cohort (visits October 2017–August 2021) and Wisconsin Registry for Alzheimer’s Prevention (WRAP) cohort (visits February 2007–November 2020) and cross-sectional data from the Sant Pau Initiative on Neurodegeneration (SPIN) cohort (baseline visits March 2009–November 2021). Participants included individuals with and without cognitive impairment grouped by amyloid and tau (AT) status using PET or CSF biomarkers. Data were analyzed from February to June 2023.

Exposures  Magnetic resonance imaging, Aβ positron emission tomography (PET), tau PET, cerebrospinal fluid (CSF) biomarkers (Aβ42/40 and p-tau immunoassays), and plasma p-tau217 (ALZpath pTau217 assay).

Main Outcomes and Measures  Accuracy of plasma p-tau217 in detecting abnormal amyloid and tau pathology, longitudinal p-tau217 change according to baseline pathology status.

Results  The study included 786 participants (mean age, 66.3 [9.7] years; 504 females [64.1%] and 282 males [35.9%]). High accuracy was observed in identifying elevated Aβ (area under the curve , 0.92-0.96; 95% CI, 0.89-0.99) and tau pathology (AUC, 0.93-0.97; 95% CI, 0.84-0.99) across all cohorts. These accuracies were comparable with CSF biomarkers in determining abnormal PET signal. The detection of abnormal Aβ pathology using a 3-range reference yielded reproducible results and reduced confirmatory testing by approximately 80%. Longitudinally, plasma p-tau217 values showed an annual increase only in Aβ-positive individuals, with the highest increase observed in those with tau positivity.

Conclusions and Relevance  This study found that a commercially available plasma p-tau217 immunoassay accurately identified biological AD, comparable with results using CSF biomarkers, with reproducible cut-offs across cohorts. It detected longitudinal changes, including at the preclinical stage.

Article Information

Accepted for Publication: November 10, 2023.

Published Online: January 22, 2024. doi:10.1001/jamaneurol.2023.5319

Open Access: This is an open access article distributed under the terms of the CC-BY License. © 2024 Ashton NJ et al. JAMA Neurology.

Corresponding Author: Nicholas J. Ashton, PhD, Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, Sahlgrenska Academy at Gothenburg University, Mölndal Hospital, Hus V3, 43180 Mölndal, Sweden (nicholas.ashton@gu.se).

Author Contributions: Dr Ashton had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis. Dr Ashton and Mr Brum contributed equally as co–first authors.

Concept and design: Ashton, Brum, Benedet, Vanmechelen, Montoliu-Gaya, Servaes, Therriault, Pascoal, Johnson, Blennow, Zetterberg.

Acquisition, analysis, or interpretation of data: Ashton, Brum, Di Molfetta, Benedet, Arslan, Jonaitis, Langhough, Cody, Wilson, Carlsson, Montoliu-Gaya, Lantero-Rodriguez, Rahmouni, Tissot, Stevenson, Therriault, Pascoal, Lleó, Alcolea, Fortea, Rosa-Neto, Johnson, Jeromin, Blennow, Zetterberg.

Drafting of the manuscript: Ashton, Brum, Arslan, Johnson.

Critical review of the manuscript for important intellectual content: Ashton, Brum, Di Molfetta, Benedet, Jonaitis, Langhough, Cody, Wilson, Carlsson, Vanmechelen, Montoliu-Gaya, Lantero-Rodriguez, Rahmouni, Tissot, Stevenson, Servaes, Therriault, Pascoal, Lleó, Alcolea, Fortea, Rosa-Neto, Johnson, Jeromin, Blennow, Zetterberg.

Statistical analysis: Ashton, Brum, Jonaitis, Therriault.

Obtained funding: Tissot, Fortea, Rosa-Neto, Johnson, Zetterberg.

Administrative, technical, or material support: Ashton, Benedet, Jonaitis, Cody, Wilson, Carlsson, Vanmechelen, Montoliu-Gaya, Rahmouni, Tissot, Stevenson, Servaes, Therriault, Lleó, Fortea, Rosa-Neto, Jeromin, Zetterberg.

Supervision: Ashton, Fortea, Blennow.

Additional Contributions: We thank Jeroen Vanbrabant, PhD, and Erik Stoops, PhD, from ADx Neuroscience, now Fujirebio, and the accelerator lab at Quanterix, for the initial prototyping of the ALZpath pTau217 assay.

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