Evidence map›Paper›PMID 42340485›Full record

ArticleActa neuropathologica2026

Tau368 improves p-tau diagnostic accuracy for FTLD-tau from FTLD-TDP.

Przemysław R Kac, Katheryn A Q Cousins, Alicja Szadziewska, Leslie M Shaw, Michael Turton, Vivianna M Van Deerlin, Peter Harrison, Henrik Zetterberg, David A Wolk, Corey T McMillan and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Acta neuropathologica, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

16 authors.

Przemysław R Kac *Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, 431 80, Mölndal, Sweden. przemyslaw.kac@gu.se.
Katheryn A Q Cousins *Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, 19104, USA.
Alicja SzadziewskaDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, 431 80, Mölndal, Sweden.
Leslie M ShawDepartment of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, 19104, USA.
Michael TurtonBioventix Plc, Farnham, GU9 7SX, UK.
Vivianna M Van DeerlinDepartment of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, 19104, USA.
Peter HarrisonBioventix Plc, Farnham, GU9 7SX, UK.
Henrik ZetterbergDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, 431 80, Mölndal, Sweden.
David A WolkDepartment of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, 19104, USA.
Corey T McMillanDepartment of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, 19104, USA.
Douglas GalaskoDepartment of Neurosciences, University of California, San Diego, CA, 92161, USA.
Jörg HanriederDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, 431 80, Mölndal, Sweden.
Edward B LeeDepartment of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, 19104, USA.
Hlin KvartsbergDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, 431 80, Mölndal, Sweden.
David J Irwin *Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, 19104, USA.
Kaj Blennow *Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, 431 80, Mölndal, Sweden.

Funding

Alzheimer's Association (#ADSF-21-831376-C, #ADSF-21-831381-C, #ADSF-21-831377-C, and #ADSF-24-1284328-CAlzheimer's Drug Discovery Foundation #201809-2016862EU Joint Programme - Neurodegenerative Disease Research JPND2021-00694Hjärnfonden #FO2022-0270Hjärnfonden #FO2024-0048-TK-130 and FO2024-0048-HK-24HORIZON EUROPE European Research Council 101053962NIH HHS P01-AG-066597, P30-AG-072979, P01-AG084497, R01-AG087258, R01AG090414, R01-NS109260Swedish Alzheimer Foundation #AF-994551Swedish State Support for Clinical Research #ALFGBG-71320Swedish state under the agreement between the Swedish government and the County Councils, the ALF-agreement #ALFGBG-1006418the European Partnership on Metrology, co-financed from the European Union's Horizon Europe Research and Innovation Programme and by the Participating States NEuroBioStand, #22HLT07the European Union's Horizon 2020 research and innovation programme under the Marie Skłodowska-Curie No 860197 (MIRIADE)UK Dementia Research Institute UKDRI-1003Vetenskapsrådet #2022-00732Vetenskapsrådet #2023-00356, #2022-01018 and #2019-02397
6 · The paper itself

Abstract

Across tauopathies-Alzheimer's disease (AD), frontotemporal lobar degeneration due to tau (FTLD-tau)-we compared cerebrospinal fluid (CSF) biomarkers of phosphorylated-tau (p-tau) p-tau181, p-tau212, tau368, total tau (t-tau), and the tau368/t-tau ratio, and tested differentiation from non-tau (FTLD-TDP, neuronal α-synuclein disease (αSyn), and controls). In AD, CSF p-tau181 and p-tau212 were significantly higher than in all other groups, including FTLD-tau, while tau368/t-tau was significantly lower. With the aim to combine tau phosphorylation biomarkers (p-tau181 and p-tau212) with biomarkers for severity of tau pathology (tau368), we made ratios between these biomarkers and examined their diagnostic accuracy in FTLD after excluding high/intermediate AD neuropathologic change (ADNC). CSF p-tau181 and p-tau212, as well as p-tau181/tau368 and p-tau212/tau368, were higher in FTLD-tau compared with non-tau groups, and the diagnostic accuracy to discriminate FTLD-tau from FTLD-TDP improved. Levels of the ratios were increased in behavioral and primary progressive aphasia variants of tauopathies when compared to FTLD-TDP. Furthermore, the biomarkers showed significant correlation with both FTLD-tau and AD tau burden at autopsy across brain regions. These results suggest unique patterns of increased relative levels of p-tau epitopes in CSF among ADNC and FTLD-tau could improve the diagnosis of tauopathies and inform inclusion criteria in clinical trial design.

Indexed as

Frontotemporal DementiaFrontotemporal Lobar Degenerationtau ProteinsAgedalpha-SynucleinAlzheimer DiseaseBiomarkersBrainFemaleHumansMaleMiddle AgedPhosphorylationTauopathiesalpha-SynucleinBiomarkersMAPT protein, humantau ProteinsAlzheimer’s diseaseBiomarkersCerebrospinal fluidFrontotemporal lobar degenerationp-TauTau368

Identifiers

PMID42340485
PMCPMC13294230

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