Evidence map›Paper›PMID 38184490›Full record

ArticleActa neuropathologica2024

CSF p-tau205: a biomarker of tau pathology in Alzheimer's disease.

Juan Lantero-Rodriguez, Laia Montoliu-Gaya, Andrea L Benedet, Agathe Vrillon, Julien Dumurgier, Emmanuel Cognat, Wagner S Brum, Nesrine Rahmouni, Jenna Stevenson, Stijn Servaes and 11 more

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in Acta neuropathologica, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
18.3field-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

48 citing papers in PubMed, 56 citations in OpenAlex.

  1. The relationship of soluble tau species with Alzheimer's disease amyloid plaque removal and tau pathology.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
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  12. Associations ofAlzheimer's & dementia : the journal of the Alzheimer's Association · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

21 authors at 8 institutions in 7 countries.

Juan Lantero-Rodriguez *Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden. juan.rodriguez.2@gu.se.ORCID http://orcid.org/0000-0002-7426-678X
Laia Montoliu-Gaya *Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Andrea L BenedetDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Agathe VrillonCognitive Neurology Center, Université de Paris Cité, GHU Nord APHP Hospital Lariboisière Fernand Widal, Paris, France.
Julien DumurgierCognitive Neurology Center, Université de Paris Cité, GHU Nord APHP Hospital Lariboisière Fernand Widal, Paris, France.
Emmanuel CognatCognitive Neurology Center, Université de Paris Cité, GHU Nord APHP Hospital Lariboisière Fernand Widal, Paris, France.
Wagner S BrumDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Nesrine RahmouniMontreal Neurological Institute, Montreal, QC, Canada.
Jenna StevensonMontreal Neurological Institute, Montreal, QC, Canada.
Stijn ServaesMontreal Neurological Institute, Montreal, QC, Canada.
Joseph TherriaultMontreal Neurological Institute, Montreal, QC, Canada.
Bruno BeckerDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Gunnar BrinkmalmDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Anniina SnellmanDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Hanna HuberDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Hlin KvartsbergDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Nicholas J AshtonDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Henrik ZetterbergDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Claire PaquetCognitive Neurology Center, Université de Paris Cité, GHU Nord APHP Hospital Lariboisière Fernand Widal, Paris, France.
Pedro Rosa-NetoMontreal Neurological Institute, Montreal, QC, Canada.
Kaj BlennowDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
University of Gothenburg · SEMontreal Neurological Institute and Hospital · CAUniversité Paris Cité · FRSahlgrenska University Hospital · SEKing's College London · GBUniversidade Federal do Rio Grande · BRUniversity of Turku · FIUniversity of Wisconsin–Madison · US

Funding

Alzheimer's Association NIRG-12-92090Alzheimer's Association NIRP-12-259245
6 · The paper itself

Abstract

Post-mortem staging of Alzheimer's disease (AD) neurofibrillary pathology is commonly performed by immunohistochemistry using AT8 antibody for phosphorylated tau (p-tau) at positions 202/205. Thus, quantification of p-tau205 and p-tau202 in cerebrospinal fluid (CSF) should be more reflective of neurofibrillary tangles in AD than other p-tau epitopes. We developed two novel Simoa immunoassays for CSF p-tau205 and p-tau202 and measured these phosphorylations in three independent cohorts encompassing the AD continuum, non-AD cases and cognitively unimpaired participants: a discovery cohort (n = 47), an unselected clinical cohort (n = 212) and a research cohort well-characterized by fluid and imaging biomarkers (n = 262). CSF p-tau205 increased progressively across the AD continuum, while CSF p-tau202 was increased only in AD and amyloid (Aβ) and tau pathology positive (A+T+) cases (P < 0.01). In A+ cases, CSF p-tau205 and p-tau202 showed stronger associations with tau-PET (r

Indexed as

Alzheimer DiseaseAmyloidogenic ProteinsAntibodiesBiomarkersHumansNeurofibrillary TanglesAmyloidogenic ProteinsAntibodiesBiomarkersAlzheimer’s diseaseBiomarkerCSFp-tau205Tau

Identifiers

PMID38184490
PMCPMC10771353
OpenAlexW4390640250

What OpenQuestion holds

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Registered trials

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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.