Evidence map›Paper›PMID 38365825›Full record

ArticleMolecular neurodegeneration2024

Plasma N-terminal containing tau fragments (NTA-tau): a biomarker of tau deposition in Alzheimer's Disease.

Juan Lantero-Rodriguez, Gemma Salvadó, Anniina Snellman, Laia Montoliu-Gaya, Wagner S Brum, Andrea L Benedet, Niklas Mattsson-Carlgren, Pontus Tideman, Shorena Janelidze, Sebastian Palmqvist and 5 more

Open access · goldAbstract read
In one paragraph

Article in Molecular neurodegeneration, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
12.7field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

32 citing papers in PubMed, 41 citations in OpenAlex.

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  20. Plasma biomarkers as core mediators in functional network abnormalities: Evidence from a two-cohort study.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors at 7 institutions in 5 countries.

Juan Lantero-Rodriguez *Department of Psychiatry and Neurochemistry, Institute of Neuroscience & Physiology, The Sahlgrenska Academy at the University of Gothenburg, House V3/SU, 43180, Mölndal, Sweden. juan.rodriguez.2@gu.se.ORCID 0000-0002-7426-678X
Gemma Salvadó *Clinical Memory Research Unit, Department of Clinical Sciences Malmö, Lund University, Lund, Sweden.
Anniina SnellmanDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience & Physiology, The Sahlgrenska Academy at the University of Gothenburg, House V3/SU, 43180, Mölndal, Sweden.
Laia Montoliu-GayaDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience & Physiology, The Sahlgrenska Academy at the University of Gothenburg, House V3/SU, 43180, Mölndal, Sweden.
Wagner S BrumDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience & Physiology, The Sahlgrenska Academy at the University of Gothenburg, House V3/SU, 43180, Mölndal, Sweden.
Andrea L BenedetDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience & Physiology, The Sahlgrenska Academy at the University of Gothenburg, House V3/SU, 43180, Mölndal, Sweden.
Niklas Mattsson-CarlgrenClinical Memory Research Unit, Department of Clinical Sciences Malmö, Lund University, Lund, Sweden.
Pontus TidemanClinical Memory Research Unit, Department of Clinical Sciences Malmö, Lund University, Lund, Sweden.
Shorena JanelidzeClinical Memory Research Unit, Department of Clinical Sciences Malmö, Lund University, Lund, Sweden.
Sebastian PalmqvistClinical Memory Research Unit, Department of Clinical Sciences Malmö, Lund University, Lund, Sweden.
Erik StomrudClinical Memory Research Unit, Department of Clinical Sciences Malmö, Lund University, Lund, Sweden.
Nicholas J AshtonDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience & Physiology, The Sahlgrenska Academy at the University of Gothenburg, House V3/SU, 43180, Mölndal, Sweden.
Henrik ZetterbergDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience & Physiology, The Sahlgrenska Academy at the University of Gothenburg, House V3/SU, 43180, Mölndal, Sweden.
Kaj BlennowDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience & Physiology, The Sahlgrenska Academy at the University of Gothenburg, House V3/SU, 43180, Mölndal, Sweden.
Oskar HanssonClinical Memory Research Unit, Department of Clinical Sciences Malmö, Lund University, Lund, Sweden. oskar.hansson@med.lu.se.
Lund University · SEUniversity of Gothenburg · SEKing's College London · GBSahlgrenska University Hospital · SEUniversidade Federal do Rio Grande · BRUniversity of Turku · FIUniversity of Wisconsin–Madison · US

Funding

AD Strategic Fund and the Alzheimer's Association ADSF-21-831376-CAD Strategic Fund and the Alzheimer's Association ADSF-21-831377-CAD Strategic Fund and the Alzheimer's Association ADSF-21-831381-CAlzheimer Drug Discovery Foundation (ADDF) 201809-2016862Alzheimer's Association 2021 Zenith Award ZEN-21-848495Alzheimer's Association 2022-2025 Grant SG-23-1038904 QCAlzheimer's Association Research Fellowship AARF-22-972612ERA PerMed ERAPERMED2021-184European Union Joint Program for Neurodegenerative Disorders JPND2019-466-236European Union Joint Programme - Neurodegenerative Disease Research JPND2021-00694European Union's Horizon 2020 research and innovation program 101061836European Union's Horizon 2020 research and innovation programme 860197Hjärnfonden ALZ2022-0006Hjärnfonden FO2017-0243Hjärnfonden FO2022-0270Knut and Alice Wallenberg foundation 2017-0383Regionalt Forskningsstöd 2022-1259Skåne University Hospital Foundation 2020-O000028Swedish Alzheimer Foundation AF-930351Swedish Alzheimer Foundation AF-939721Swedish Alzheimer Foundation AF-968270Swedish Alzheimer Foundation AF-980907Swedish Brain Foundation FO2021-0293Swedish federal government under the ALF agreement 2022-Projekt0080Swedish Research Council 2017-00915Swedish Research Council 2019-02397Swedish Research Council 2022-00732Swedish Research Council 2022-00775Swedish Research Council 2022-01018Swedish State Support for Clinical Research ALFGBG-71320Swedish state under the agreement between the Swedish government and the County Councils, the ALF-agreement ALFGBG-715986Swedish state under the agreement between the Swedish government and the County Councils, the ALF-agreement ALFGBG-965240The Parkinson foundation of Sweden 1412/22UK Dementia Research Institute at UCL UKDRI-1003uropean Union's Horizon Europe research and innovation programme 101053962
6 · The paper itself

Abstract

backgroundNovel phosphorylated-tau (p-tau) blood biomarkers (e.g., p-tau181, p-tau217 or p-tau231), are highly specific for Alzheimer's disease (AD), and can track amyloid-β (Aβ) and tau pathology. However, because these biomarkers are strongly associated with the emergence of Aβ pathology, it is difficult to determine the contribution of insoluble tau aggregates to the plasma p-tau signal in blood. Therefore, there remains a need for a biomarker capable of specifically tracking insoluble tau accumulation in brain.

methodsNTA is a novel ultrasensitive assay targeting N-terminal containing tau fragments (NTA-tau) in cerebrospinal fluid (CSF) and plasma, which is elevated in AD. Using two well-characterized research cohorts (BioFINDER-2, n = 1,294, and BioFINDER-1, n = 932), we investigated the association between plasma NTA-tau levels and disease progression in AD, including tau accumulation, brain atrophy and cognitive decline.

resultsWe demonstrate that plasma NTA-tau increases across the AD continuum¸ especially during late stages, and displays a moderate-to-strong association with tau-PET (β = 0.54, p < 0.001) in Aβ-positive participants, while weak with Aβ-PET (β = 0.28, p < 0.001). Unlike plasma p-tau181, GFAP, NfL and t-tau, tau pathology determined with tau-PET is the most prominent contributor to NTA-tau variance (52.5% of total R

conclusionOur results indicate that plasma NTA-tau levels increase across the AD continuum, especially during mid-to-late AD stages, and it is closely associated with in vivo tau tangle deposition in AD and its downstream effects. Moreover, this novel biomarker has potential as a cost-effective and easily accessible tool for monitoring disease progression and cognitive decline in clinical settings, and as an outcome measure in clinical trials which also need to assess the downstream effects of successful Aβ removal.

Indexed as

Alzheimer DiseaseCognitive DysfunctionAmyloid beta-PeptidesAtrophyBiomarkersDisease ProgressionHumansPositron-Emission Tomographytau ProteinsAmyloid beta-PeptidesBiomarkerstau ProteinsAlzheimer’s diseaseBioFINDERBiomarkersNTANTA-tauPlasmaTauTau pathologyTau-PET

Identifiers

PMID38365825
PMCPMC10874032
OpenAlexW4391913688

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.