Evidence map›Paper›PMID 40140924›Full record

ArticleAlzheimer's research & therapy2025

Diagnostic performance of plasma p-tau217 in a memory clinic cohort using the Lumipulse automated platform.

Francisco Martínez-Dubarbie, Armando Guerra-Ruiz, Sara López-García, Carmen Lage, Marta Fernández-Matarrubia, Álvaro Nevado-Cáceres, María Rivera-Sánchez, Andrea Valera-Barrero, Ana Pozueta-Cantudo, María García-Martínez and 10 more

Abstract read
In one paragraph

Article in Alzheimer's research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

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

16 citing papers in PubMed.

  1. Article
  2. Multicenter validation of plasma p-tau217/ amyloid beta 1-42 ratio in symptomatic Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
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  4. Review
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  12. Review
  13. A modelling approach to derive population-specific cutoff for plasma p-Tau217.The journal of prevention of Alzheimer's disease · 2025
    Article
  14. Article
  15. Article
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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

20 authors.

Francisco Martínez-DubarbieNeurology Service, Marqués de Valdecilla University Hospital, Avda. de Valdecilla 25, Santander, Cantabria, 39008, Spain. dubarmar@hotmail.com.
Armando Guerra-RuizBiochemistry and Clinical Analysis Department, Marqués de Valdecilla University Hospital, Santander, Cantabria, 39008, Spain.
Sara López-GarcíaNeurology Service, Marqués de Valdecilla University Hospital, Avda. de Valdecilla 25, Santander, Cantabria, 39008, Spain.
Carmen LageNeurology Service, Marqués de Valdecilla University Hospital, Avda. de Valdecilla 25, Santander, Cantabria, 39008, Spain.
Marta Fernández-MatarrubiaNeurology Service, Marqués de Valdecilla University Hospital, Avda. de Valdecilla 25, Santander, Cantabria, 39008, Spain.
Álvaro Nevado-CáceresNeurology Service, Marqués de Valdecilla University Hospital, Avda. de Valdecilla 25, Santander, Cantabria, 39008, Spain.
María Rivera-SánchezNeurology Service, Marqués de Valdecilla University Hospital, Avda. de Valdecilla 25, Santander, Cantabria, 39008, Spain.
Andrea Valera-BarreroNeurology Service, Marqués de Valdecilla University Hospital, Avda. de Valdecilla 25, Santander, Cantabria, 39008, Spain.
Ana Pozueta-CantudoNeurology Service, Marqués de Valdecilla University Hospital, Avda. de Valdecilla 25, Santander, Cantabria, 39008, Spain.
María García-MartínezNeurology Service, Marqués de Valdecilla University Hospital, Avda. de Valdecilla 25, Santander, Cantabria, 39008, Spain.
Andrea Corrales-PardoNeurology Service, Marqués de Valdecilla University Hospital, Avda. de Valdecilla 25, Santander, Cantabria, 39008, Spain.
María BravoNeurology Service, Marqués de Valdecilla University Hospital, Avda. de Valdecilla 25, Santander, Cantabria, 39008, Spain.
Marcos López-HoyosInstitute for Research Marqués de Valdecilla (IDIVAL), Santander, Cantabria, 39011, Spain.
Juan Irure-VenturaInstitute for Research Marqués de Valdecilla (IDIVAL), Santander, Cantabria, 39011, Spain.
Enrique Marco de LucasInstitute for Research Marqués de Valdecilla (IDIVAL), Santander, Cantabria, 39011, Spain.
Marta Drake-PérezInstitute for Research Marqués de Valdecilla (IDIVAL), Santander, Cantabria, 39011, Spain.
Nancy Heidy Cahuana-SantamaríaBiochemistry and Clinical Analysis Department, Marqués de Valdecilla University Hospital, Santander, Cantabria, 39008, Spain.
María Teresa García-UnzuetaInstitute for Research Marqués de Valdecilla (IDIVAL), Santander, Cantabria, 39011, Spain.
Pascual Sánchez-JuanCIBERNED, Network Center for Biomedical Research in Neurodegenerative Diseases, National Institute of Health Carlos III, Madrid, 28220, Spain.
Eloy Rodríguez-RodríguezNeurology Service, Marqués de Valdecilla University Hospital, Avda. de Valdecilla 25, Santander, Cantabria, 39008, Spain.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPlasma biomarkers for Alzheimer's disease (AD) are a promising tool for accessible and accurate biological diagnostics. However, data in clinical practice are needed to better understand their diagnostic and prognostic ability in memory unit patients.

methodsWe analyzed plasma phosphorylated tau at threonine 217 (p-tau217) and neuroflament light chain (NfL) levels and AD cerebrospinal fluid (CSF) biomarkers in a group of 493 subjects using the Lumipulse G600II platform. The sample includes 340 patients from our memory unit (142 dementia, 186 mild cognitive impairment, and 12 with subjective complaints) and 153 cognitively unimpaired volunteers. We have correlated plasma and CSF biomarkers; we have analyzed plasma biomarker levels as a function of clinical diagnosis, cognitive status and amyloid status. We have also studied the ability of p-tau217 to discriminate between amyloid-positive and -negative subjects according to CSF using receiver operating characteristic curves.

resultsPlasma p-tau217 correlated significantly with CSF Aβ42/Aβ40 (Rho = -0.75; p-value < 0.001), p-tau181 (r = 0.66; p-value < 0.001), and t-tau (r = 0.59; p-value < 0.001). Plasma NfL correlated with CSF NfL (r = 0.48; p-value < 0.001). By clinical diagnosis, plasma p-tau217 levels showed to be higher in AD patients than in healthy controls (difference = 0.63 pg/ml; p-value < 0.001), FTD (difference = 0.60 pg/ml; p-value < 0.001), and nondegenerative dementias (difference = 0.61 pg/ml; p-value < 0.001). Plasma p-tau217 showed an area under the curve of 0.95 to discriminate between A + and A- subjects (95%CI 0.93-0.97).

conclusionPlasma p-tau217 shows excellent results for detecting amyloid pathology at brain level in a clinical setting with an AUC of 0.95. It is a highly specific marker of AD and increases progressively along the disease continuum. Using plasma p-tau217 as an initial diagnostic tool with cut-offs at sensitivities and specificities of 95 or 97.5% could save between 57.4-84.8% of LP/PETs with diagnostic accuracies of 95-97%. Plasma NfL increases progressively at different cognitive stages.

Indexed as

Alzheimer DiseaseCognitive Dysfunctiontau ProteinsAgedAged, 80 and overAmyloid beta-PeptidesBiomarkersCohort StudiesFemaleHumansMaleMiddle AgedNeurofilament ProteinsPeptide FragmentsPhosphorylationROC CurveAmyloid beta-PeptidesBiomarkersMAPT protein, humanneurofilament protein LNeurofilament ProteinsPeptide Fragmentstau ProteinsAlzheimer’s diseaseBiomarkersCross-sectionalEarly diagnosisHealthy controlsPlasma p-tau217

Identifiers

PMID40140924
PMCPMC11948696

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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.