Evidence map›Paper›PMID 32725127›Full record

ArticleThe Journal of experimental medicine2020

Blood plasma phosphorylated-tau isoforms track CNS change in Alzheimer's disease.

Nicolas R Barthélemy, Kanta Horie, Chihiro Sato, Randall J Bateman

Open access · greenAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 287 papers, 7 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
287citing papers in PubMed, 7 pooled it
30.5field-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

287 citing papers in PubMed, 7 syntheses or guidelines pooled it, 421 citations in OpenAlex.

  1. Pooled it
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  7. Pooled it
  8. Pharmacodynamic effects of semorinemab on plasma and CSF biomarkers of Alzheimer's disease pathophysiology.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Trial
  9. Article
  10. APOE ε4 accelerates plasma p-tau217 trajectory: a Bayesian joint longitudinal analysis of ADNI.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
    Article
  11. Article
  12. Article
  13. [European journal of nuclear medicine and molecular imaging · 2026
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Lung endothelial cytopathic tau is sufficient to impair long-term potentiation during infection.American journal of respiratory cell and molecular biology · 2026
    Article
  19. Observational
  20. Predicting continuous amyloid PET levels with CSF and plasma brain-derived p-tau217.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article

227 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Nicolas R BarthélemyDepartment of Neurology, Washington University School of Medicine, St. Louis, MO.
Kanta HorieDepartment of Neurology, Washington University School of Medicine, St. Louis, MO.
Chihiro SatoDepartment of Neurology, Washington University School of Medicine, St. Louis, MO.
Randall J BatemanDepartment of Neurology, Washington University School of Medicine, St. Louis, MO.
Washington University in St. Louis · US

Funding

WASHINGTON UNIVERSITY ALZHEIMERS DISEASE RESEARCH CENTERP50AG005681 · NIA · WASHINGTON UNIVERSITY · PI MORRIS, JOHN · 1985 to 2019
$52.1M
Research Education ComponentP30AG066444 · NIA · WASHINGTON UNIVERSITY · PI DAVID M. HOLTZMAN · 2020 to 2026
$28.7M
CNS TAU KINETICS IN ALZHEIMER'S DISEASER01NS095773 · NINDS · WASHINGTON UNIVERSITY · PI BATEMAN, RANDALL J · 2016 to 2020
$3.6M
NIA NIH HHS P30 AG066444NIA NIH HHS P50 AG005681NINDS NIH HHS R01 NS095773
6 · The paper itself

Abstract

Highly sensitive and specific plasma biomarkers for Alzheimer's disease (AD) have the potential to improve diagnostic accuracy in the clinic and facilitate research studies including enrollment in prevention and treatment trials. We recently reported CSF tau hyperphosphorylation, especially on T217, is an accurate predictor of β-amyloidosis at asymptomatic and symptomatic stages. In the current study, we determine by mass spectrometry the potential utility of plasma p-tau isoforms to detect AD pathology and investigate CSF and plasma tau isoforms' profile relationships. Plasma tau was truncated as previously described in CSF. CSF and plasma measures of p-tau-217 and p-tau-181 were correlated. No correlation was found between CSF and plasma on total-tau levels and pS202 measures. We found p-tau-217 and p-tau-181 were highly specific for amyloid plaque pathology in the discovery cohort (n = 36, AUROC = 0.99 and 0.98 respectively). In the validation cohort (n = 92), p-tau-217 measures were still specific to amyloid status (AUROC = 0.92), and p-tau-181 measures were less specific (AUROC = 0.75).

Indexed as

AdultAgedAged, 80 and overAlzheimer DiseaseAmyloid beta-PeptidesBiomarkersBrainCase-Control StudiesCohort StudiesFemaleHumansMaleMass SpectrometryMiddle AgedPhosphorylationPlaque, AmyloidAmyloid beta-PeptidesBiomarkersProtein Isoformstau Proteins

Identifiers

PMID32725127
PMCPMC7596823
OpenAlexW3045987239

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

None linked

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.