Evidence map›Paper›PMID 38970274›Full record

ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2024

Longitudinal plasma phosphorylated-tau217 and other related biomarkers in a non-demented Alzheimer's risk-enhanced sample.

Lianlian Du, Rebecca E Langhough, Rachael E Wilson, Ramiro Eduardo Rea Reyes, Bruce P Hermann, Erin M Jonaitis, Tobey J Betthauser, Nathaniel A Chin, Bradley Christian, Lauren Chaby and 8 more

Abstract read
In one paragraph

Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 3 pooled it
–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

28 citing papers in PubMed, 3 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Article
  6. Plasma p-tau markers, vascular factors, and cognitive decline in the CIMA-Q cohort.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  7. Predicting Preclinical Cognitive Decline Using Plasma P-tau217 andmedRxiv : the preprint server for health sciences · 2026
    Article
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  14. Lifestyle, genetic risk, plasma pTau217, and incident cognitive impairment in WRAP.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  15. Article
  16. The performance of plasma p-tau217 in Black middle-aged and older adults.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
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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

18 authors.

Lianlian DuWisconsin Alzheimer's Disease Research Center, Department of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, USA.ORCID 0000-0002-1662-0883
Rebecca E LanghoughWisconsin Alzheimer's Disease Research Center, Department of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, USA.
Rachael E WilsonWisconsin Alzheimer's Disease Research Center, Department of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, USA.
Ramiro Eduardo Rea ReyesWisconsin Alzheimer's Disease Research Center, Department of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, USA.
Bruce P HermannWisconsin Alzheimer's Disease Research Center, Department of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, USA.
Erin M JonaitisWisconsin Alzheimer's Disease Research Center, Department of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, USA.
Tobey J BetthauserWisconsin Alzheimer's Disease Research Center, Department of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, USA.
Nathaniel A ChinWisconsin Alzheimer's Disease Research Center, Department of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, USA.
Bradley ChristianWaisman Laboratory for Brain Imaging and Behavior, University of Wisconsin-Madison, Madison, Wisconsin, USA.
Lauren ChabyALZpath, Inc., Carlsbad, California, USA.
Andreas JerominALZpath, Inc., Carlsbad, California, USA.
Guglielmo Di MolfettaDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Wagner S BrumDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Burak ArslanDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Nicholas AshtonDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Kaj BlennowDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Henrik ZetterbergWisconsin Alzheimer's Disease Research Center, Department of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, USA.
Sterling C JohnsonWisconsin Alzheimer's Disease Research Center, Department of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, USA.ORCID 0000-0002-8501-545X

Funding

Wisconsin Registry for Alzheimer's Prevention: Sex Differences in DNA MethylationR01AG027161 · NIA · UNIVERSITY OF WISCONSIN-MADISON · PI Nathaniel Ark Chin, Sterling C Johnson · 2007 to 2026
$35.6M
The Longitudinal Course of Neural Function and Amyloid in People At Risk for ADR01AG021155 · NIA · UNIVERSITY OF WISCONSIN-MADISON · PI Sterling C Johnson · 2004 to 2026
$27.0M
Wisconsin Registry for Alzheimer's PreventionRF1AG027161 · NIA · UNIVERSITY OF WISCONSIN-MADISON · PI JOHNSON, STERLING C · 2018 to 2018
$18.8M
AARFNIA NIH HHS R01 AG021155NIA NIH HHS R01 AG027161NIA NIH HHS RF1 AG027161NIHNIH RO1AG021155R01AG027161Swedish State Support for Clinical Research #ALFGBG-71320the AD Strategic Fund and the Alzheimer's Association #ADSF-21-831376-Cthe AD Strategic Fund and the Alzheimer's Association #ADSF-21-831377-Cthe AD Strategic Fund and the Alzheimer's Association #ADSF-21-831381-Cthe AD Strategic Fund and the Alzheimer's Association #ADSF-24-1284328-Cthe Alzheimer's Drug Discovery Foundation (ADDF), USA #201809-2016862the European Union's Horizon Europe research and innovationthe Marie Skłodowska-Curie No. 860197the Swedish Research Council #2019-02397the Swedish Research Council #2022-01018the Swedish Research Council #2023-00356
6 · The paper itself

Abstract

introductionUnderstanding longitudinal change in key plasma biomarkers will aid in detecting presymptomatic Alzheimer's disease (AD).

methodsSerial plasma samples from 424 Wisconsin Registry for Alzheimer's Prevention participants were analyzed for phosphorylated-tau217 (p-tau217; ALZpath) and other AD biomarkers, to study longitudinal trajectories in relation to disease, health factors, and cognitive decline. Of the participants, 18.6% with known amyloid status were amyloid positive (A+); 97.2% were cognitively unimpaired (CU).

resultsIn the CU, amyloid-negative (A-) subset, plasma p-tau217 levels increased modestly with age but were unaffected by body mass index and kidney function. In the whole sample, average p-tau217 change rates were higher in those who were A+ (e.g., simple slopes(se) for A+ and A- at age 60 were 0.232(0.028) and 0.038(0.013))). High baseline p-tau217 levels predicted faster preclinical cognitive decline. DISCUSSION: p-tau217 stands out among markers for its strong association with disease and cognitive decline, indicating its potential for early AD detection and monitoring progression. HIGHLIGHTS: Phosphorylated-tau217 (p-tau217) trajectories were significantly different in people who were known to be amyloid positive. Subtle age-related trajectories were seen for all the plasma markers in amyloid-negative cognitively unimpaired. Kidney function and body mass index were not associated with plasma p-tau217 trajectories. Higher plasma p-tau217 was associated with faster preclinical cognitive decline.

Indexed as

Alzheimer DiseaseBiomarkerstau ProteinsAgedCognitive DysfunctionDisease ProgressionFemaleHumansLongitudinal StudiesMaleMiddle AgedPhosphorylationBiomarkerstau ProteinsALZpathbiomarkersBMIcognitive compositeplasmapreclinical Alzheimer's disease

Identifiers

PMID38970274
PMCPMC11497664

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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.