Evidence map›Paper›PMID 41929322›Full record

ArticlemedRxiv : the preprint server for health sciences2026

Plasma pTau217 as a Prognostic, Monitoring, and Risk-Stratification Biomarker of Clinical Progression in Lewy Body Disease.

S A Lorkiewicz, C Abdelnour, M Bolen, A M Smith, M Shahid-Besanti, D Hemachandra, E M Müller-Oehring, N Siddiqui, L Montoliu-Gaya, B Arslan and 8 more

Abstract readPreprint
In one paragraph

Article in medRxiv : the preprint server for health sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the 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.

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

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

18 authors.

S A LorkiewiczDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.ORCID 0000-0002-0560-5979
C AbdelnourDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.
M BolenDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.ORCID 0000-0003-1973-3784
A M SmithDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.
M Shahid-BesantiDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.ORCID 0000-0002-8515-3238
D HemachandraDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.
E M Müller-OehringDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.ORCID 0000-0001-8908-4471
N SiddiquiDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.
L Montoliu-GayaDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, University of Gothenburg, Mölndal, Sweden.
B ArslanDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, University of Gothenburg, Mölndal, Sweden.
N J AshtonDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, University of Gothenburg, Mölndal, Sweden.ORCID 0000-0002-3579-8804
E N WilsonDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.
L TianDepartment of Epidemiology and Population Health, Stanford University School of Medicine, Stanford, CA, USA.
K I AndreassonDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.ORCID 0000-0001-8391-4155
E C MorminoDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.
V W HendersonDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.
H ZetterbergDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, University of Gothenburg, Mölndal, Sweden.
K L PostonDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.ORCID 0000-0003-3424-7143

Funding

Stanford Alzheimer's Disease Research CenterAdmin Supp: Developing iPSC models for AD and PDP30AG066515 · NIA · STANFORD UNIVERSITY · PI Lisa Goldman Rosas · 2020 to 2026
$29.0M
Project 4: Novel reagent development to enable molecular characterizationU19AG065156 · NIA · UNIVERSITY OF WASHINGTON · PI TIAN, LU · 2020 to 2024
$15.9M
Neural mechanisms of gait disturbances as individualized digital biomarker trajectories in preclinical dementiaR01AG089169 · NIA · STANFORD UNIVERSITY · PI Ehsan Adeli · 2024 to 2026
$4.5M
The impact of early Tau pathology on cognitive progression and neuropsychiatric symptoms in Parkinson's diseaseR01NS115114 · NINDS · STANFORD UNIVERSITY · PI ANDREASSON, KATRIN I., POSTON, KATHLEEN LOMBARD · 2019 to 2023
$4.2M
Neurofunctional Mechanisms of Changes in Cognition and Motor Function in Aging with HIV and Parkinson's DiseaseR01AG081144 · NIA · SRI INTERNATIONAL · PI TILMAN SCHULTE · 2023 to 2026
$3.2M
ENIGMA Parkinson’s Initiative: A Global Initiative for Parkinson’s DiseaseR01NS107513 · NINDS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI POSTON, KATHLEEN LOMBARD, THOMPSON, PAUL M · 2021 to 2025
$3.2M
Role of altered gut immune response in Lewy Body DiseaseU01DK140939 · NIDDK · STANFORD UNIVERSITY · PI Laren Becker, Kathleen Lombard Poston · 2024 to 2026
$2.2M
Glymphatic MR Imaging and Biomarker Discovery in Aging with HIV InfectionR21AG096957 · NIA · SRI INTERNATIONAL · PI MULLER-OEHRING, EVA M · 2025 to 2025
$630k
Free water imaging in PDR21NS132101 · NINDS · STANFORD UNIVERSITY · PI POSTON, KATHLEEN LOMBARD · 2023 to 2023
$501k
NIA NIH HHS P30 AG066515NIA NIH HHS R01 AG081144NIA NIH HHS R01 AG089169NIA NIH HHS R21 AG096957NIA NIH HHS U19 AG065156NIDDK NIH HHS U01 DK140939NINDS NIH HHS R01 NS107513NINDS NIH HHS R01 NS115114NINDS NIH HHS R21 NS132101
6 · The paper itself

Abstract

Background and Objectives: In Lewy body disease (LBD), co-occurring Alzheimer's disease (AD) neuropathologic change (ADNC) is associated with worse clinical outcomes. While plasma pTau217 detects ADNC in LBD, its prognostic, monitoring, and risk-stratification utility remains unclear. We evaluated whether plasma pTau217 predicted cognitive and functional decline and risk for progression to MCI or dementia in LBD. Methods: We included 501 participants enrolled in the Stanford Alzheimer's Disease Research Center with plasma pTau217 data who were clinically diagnosed as LBD spectrum ( Results: In LBD, higher continuous baseline plasma pTau217 predicted accelerated CDR-SB increase ( Discussion: Plasma pTau217 is a promising prognostic, monitoring, and risk stratification biomarker of clinical progression in LBD, underscoring its utility in mixed pathology groups for clinical practice and trials.

Indexed as

cognitive declinedementiaLewy body diseaseParkinson’s diseaseplasma biomarkerspTau217

Identifiers

PMID41929322
PMCPMC13042093

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.