Evidence map›Paper›PMID 40373247›Full record

Observational studyNeurology2025

Associations Between Changes in Levels of Phosphorylated Tau and Severity of Cognitive Impairment in Early Alzheimer Disease.

Fernando Gonzalez-Ortiz, Bjørn-Eivind Kirsebom, Yara Yakoub, Julia K Gundersen, Lene Pålhaugen, Knut Waterloo, Per Selnes, Jonas Alexander Jarholm, Berglind Gísladóttir, Arvid Rongve and 9 more

Abstract readObservational Study
In one paragraph

Observational study in Neurology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

  1. Interpreting p-tau217 on the ward: frailty and plasma biomarkers in acutely admitted older adults.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  2. Article
  3. Article
  4. Article
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  6. The roles of biomarkers in Alzheimer's disease clinical trials.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
    Review
  7. Article
  8. Article
  9. Observational
  10. Article
  11. Repeated plasma p-tau217 measurements to monitor clinical progression heterogeneity.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  12. 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

19 authors.

Fernando Gonzalez-OrtizInst. of Neuroscience and Physiology, University of Gothenburg, Mölndal, Sweden.ORCID 0000-0001-7897-9456
Bjørn-Eivind KirsebomDepartment of Neurology, University Hospital of North Norway, Tromsø, Norway.ORCID 0000-0002-1413-9578
Yara YakoubDouglas Mental Health University Institute, Centre for Studies on the Prevention of Alzheimer's Disease (StoP-AD), Montreal, Quebec, Canada.
Julia K GundersenDepartment of Neurology, Akershus University Hospital, Lørenskog, Norway.
Lene PålhaugenDepartment of Neurology, Akershus University Hospital, Lørenskog, Norway.
Knut WaterlooDepartment of Neurology, University Hospital of North Norway, Tromsø, Norway.
Per SelnesDepartment of Neurology, Akershus University Hospital, Lørenskog, Norway.
Jonas Alexander JarholmDepartment of Neurology, Akershus University Hospital, Lørenskog, Norway.
Berglind GísladóttirDepartment of Neurology, Akershus University Hospital, Lørenskog, Norway.
Arvid RongveDepartment of Neuropsychology, Haugesund Hospital, Norway.ORCID 0000-0002-0476-4134
Ragnhild Eide SkogsethDepartment of Geriatric Medicine, Haraldsplass Deaconess Hospital, Bergen, Norway.
Geir BråthenDepartment of Neurology and Clinical Neurophysiology, University Hospital of Trondheim, Norway.
Dag AarslandCentre for Age-Related Diseases. Stavanger University Hospital Stavanger, Norway.ORCID 0000-0001-6314-216X
Michael TurtonBioventix Plc, Surrey, United Kingdom.
Peter HarrisonBioventix Plc, Surrey, United Kingdom.
Henrik ZetterbergInst. of Neuroscience and Physiology, University of Gothenburg, Mölndal, Sweden.ORCID 0000-0003-3930-4354
Sylvia VilleneuveDouglas Mental Health University Institute, Centre for Studies on the Prevention of Alzheimer's Disease (StoP-AD), Montreal, Quebec, Canada.ORCID 0000-0003-2338-0467
Tormod FladbyDepartment of Neurology, Akershus University Hospital, Lørenskog, Norway.ORCID 0000-0002-9984-9797
Kaj BlennowInst. of Neuroscience and Physiology, University of Gothenburg, Mölndal, Sweden.ORCID 0000-0002-1890-4193

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

objectivesAligning biomarker evidence with clinical presentation in early Alzheimer disease (AD) is essential for improving diagnosis, prognosis, and interventions. This study evaluates the relationship between cognitive impairment, future decline, and phosphorylated tau levels in plasma and CSF in predementia AD.

methodsThis longitudinal observational study included predementia cases and controls from 2 independent cohorts: the Norwegian Dementia Disease Initiation (DDI) and Canadian Pre-Symptomatic Evaluation of Experimental or Novel Treatments for Alzheimer's Disease (PREVENT-AD). In DDI, cognitively normal (CN) and mild cognitive impairment (MCI) cases were classified using CSF Aβ42/40 ratio (A) and p-tau181 (T), whereas classification in PREVENT-AD (A) was based on amyloid PET scans. In DDI, we assessed CSF-plasma correlations for p-tau181, p-tau217, and p-tau231. Diagnostic accuracies were evaluated through receiver operating characteristic analyses. Linear mixed models evaluated p-tau associations with future memory decline. Between-group differences in plasma p-tau217 were assessed in both cohorts.

resultsIn DDI (n = 431), participants were classified as CN A-/T- (n = 169), A+/T- (CN = 26, MCI = 24), A+/T+ (CN = 40, MCI = 105), and A-/T+ (CN = 34, MCI = 33), with a mean age of 64.1 years and 55.9% female. In PREVENT-AD (n = 190), participants were categorized as CN A- (n = 118), CN A+ (n = 49), and MCI A+ (n = 21), with a mean age of 67.8 years and 72.6% female. In DDI, plasma p-tau217 showed high accuracy in identifying A+ participants (areas under the curve [AUC]: 0.85) and a moderate correlation with CSF p-tau217 (rho = 0.65, DISCUSSION: Our findings suggest that, unlike p-tau181 and p-tau231, plasma p-tau217 consistently aligns with cognitive status in A+ individuals and better reflects CSF biomarker abnormalities, reducing discrepancies between clinical and biochemical findings. Its association with baseline and future memory decline highlights its diagnostic and prognostic value, particularly when CSF analysis or PET is unavailable.

Indexed as

Alzheimer DiseaseCognitive Dysfunctiontau ProteinsAgedAged, 80 and overAmyloid beta-PeptidesBiomarkersFemaleHumansLongitudinal StudiesMaleMiddle AgedPeptide FragmentsPhosphorylationPositron-Emission TomographySeverity of Illness IndexAmyloid beta-PeptidesBiomarkersMAPT protein, humanPeptide Fragmentstau Proteins

Identifiers

PMID40373247
PMCPMC12083872

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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.