Evidence map›Paper›PMID 42615578›Full record

Observational studyEuropean journal of neurology2026

Plasma Profile of Brain-Derived Tau After Ischemic Stroke.

Karl Sjölin, Björn Röyter, Bianka Forgo, Julia Aulin, Kim Kultima, Johan Lindbäck, Jakob O Ström, Joachim Burman

Registry-linked trialAbstract readObservational Study
In one paragraph

Observational study in European journal of neurology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03812666 (Inflammatory Biomarkers In Stroke - Discovery Phase), which is not on this map. Not yet cited in PubMed.

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

NCT03812666 unknown statusnot on this map

Inflammatory Biomarkers In Stroke - Discovery Phase

TypeobservationalSponsorJakob StrömRan2019 to 2025Enrolled200ConditionsStroke, Acute, Pneumonia, Bacterial
3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

8 authors.

Karl SjölinDepartment of Medical Sciences, Translational Neurology, Uppsala University, Uppsala, Sweden.ORCID https://orcid.org/0000-0002-6693-1348
Björn RöyterDepartment of Obstetrics and Gynecology, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
Bianka ForgoDepartment of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden.ORCID https://orcid.org/0000-0003-0627-1795
Julia AulinDepartment of Medical Sciences, Translational Neurology, Uppsala University, Uppsala, Sweden.ORCID https://orcid.org/0000-0002-9193-5068
Kim KultimaDepartment of Medical Sciences, Clinical Chemistry, Uppsala University, Uppsala, Sweden.ORCID https://orcid.org/0000-0002-0680-1410
Johan LindbäckUppsala Clinical Research Center (UCR), Uppsala University, Uppsala, Sweden.ORCID https://orcid.org/0000-0002-6473-8798
Jakob O StrömDepartment of Neurology, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
Joachim BurmanDepartment of Medical Sciences, Translational Neurology, Uppsala University, Uppsala, Sweden.ORCID https://orcid.org/0000-0002-7045-1806

Funding

Bissen Brainwalk FoundationNyckelfondenRegionala Forskningsrådet Uppsala/ÖrebroResearch Committee at Örebro University HospitalSwedish state support for research (ALF agreement)
6 · The paper itself

Abstract

BACKGROUND AND

aimBrain-derived tau (BD-tau) is a predominantly CNS-derived form of tau protein detectable in blood that reflects brain injury and has emerged as a potential biomarker in ischemic stroke for assessing neuronal damage, monitoring infarct progression, and predicting functional outcome. However, its temporal profile and the optimal timing for correlation with infarct volume remain unclear.

methodsThis prospective cohort study included patients with ischemic stroke, with venous blood samples collected daily during the first week and at 3 months after symptom onset. Infarct volume was assessed by MRI at 48-72 h. Plasma BD-tau concentrations were measured using a Simoa assay. Linear mixed-effects models were used to analyze changes in biomarker levels. The optimal time point for correlation between BD-tau and infarct volume was identified using a 24-h moving-window Pearson correlation analysis.

resultsFifty-four patients (median age 78 years, 50% female) contributed 285 plasma samples. Plasma levels of BD-tau followed a parabolic trajectory reaching a peak approximately 5 days after symptom onset. After 90 days, the concentration of BD-tau was lower than in the last measurement of the first week. The strongest correlation between BD-tau and infarct volume occurred at 105 h (4.4 days) (r = 0.89, 95% CI: 0.78-0.95) after symptom onset.

conclusionsPlasma BD-tau exhibits a distinct temporal profile after ischemic stroke, with peak levels and maximal correlation with infarct volume occurring around Day 4-5. These findings have important implications for interpreting BD-tau levels and optimizing sampling strategies in clinical studies.

trial registrationClinicaltrials.gov NCT03812666.

Indexed as

BrainBrain IschemiaIschemic Stroketau ProteinsAgedAged, 80 and overBiomarkersFemaleHumansMagnetic Resonance ImagingMaleMiddle AgedProspective StudiesBiomarkerstau ProteinsBD‐taubiomarkersstroke

Identifiers

PMID42615578
PMCPMC13488363

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Registered trials

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.