Evidence map›Paper›PMID 38888142›Full record

ArticleAnnals of neurology2024

Plasma pTau181 Reveals a Pathological Signature that Predicts Cognitive Outcomes in Lewy Body Disease.

Carla Abdelnour, Christina B Young, Marian Shahid-Besanti, Alena Smith, Edward N Wilson, Javier Ramos Benitez, Hillary Vossler, Melanie J Plastini, Joseph R Winer, Geoffrey A Kerchner and 8 more

Abstract read
In one paragraph

Article in Annals of neurology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. Loss of neuronal population organization links pathology to behavior in a model of Alzheimer's disease.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Plasma Phosphorylated Tau181 as a Biomarker for Alzheimer's Disease Co-Pathology in Lewy Body Disease.Movement disorders : official journal of the Movement Disorder Society · 2025
    Article
  8. 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

18 authors.

Carla AbdelnourDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.ORCID 0000-0002-7636-9758
Christina B YoungDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.
Marian Shahid-BesantiDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.ORCID 0000-0002-8515-3238
Alena SmithDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.
Edward N WilsonDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.ORCID 0000-0003-0640-5247
Javier Ramos BenitezDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.
Hillary VosslerDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.
Melanie J PlastiniDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.ORCID 0000-0003-2011-7882
Joseph R WinerDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.ORCID 0000-0003-4069-3158
Geoffrey A KerchnerPharma Research and Early Development, F. Hoffmann-La Roche, Ltd., Basel, Switzerland.
Brenna CholertonDepartment of Pathology, Stanford University School of Medicine, Stanford, CA, USA.
Katrin I AndreassonDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.
Victor W HendersonDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.
Maya YutsisDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.
Thomas J MontineDepartment of Pathology, Stanford University School of Medicine, Stanford, CA, USA.
Lu TianDepartment of Biomedical Data Science, School of Medicine, Department of Statistics, School of Humanities and Sciences, Stanford University, Stanford, CA, USA.
Elizabeth C MorminoDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.
Kathleen L PostonDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.ORCID 0000-0003-3424-7143

Funding

National Centralized Repository for Alzheimer's Disease and Related Dementias (NCRAD)U24AG021886 · NIA · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI TATIANA M. FOROUD · 2002 to 2026
$119.8M
Stanford Alzheimer's Disease Research CenterAdmin Supp: Developing iPSC models for AD and PDP30AG066515 · NIA · STANFORD UNIVERSITY · PI Michael D Greicius · 2020 to 2026
$29.0M
Udall Center Director's meeting poster awardP50NS062684 · NINDS · UNIVERSITY OF WASHINGTON · PI MONTINE, THOMAS J · 2009 to 2020
$18.3M
Working Memory in Parkinson Disease: A Cognitive & Systems Neuroscience ApproachP50AG047366 · NIA · STANFORD UNIVERSITY · PI HENDERSON, VICTOR · 2015 to 2019
$7.9M
Hippocampal-dependent memory decline in aging and early Alzheimer's diseaseR01AG074339 · NIA · STANFORD UNIVERSITY · PI ELIZABETH MORMINO · 2022 to 2026
$6.0M
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
Neuropathology of synapses in AD and ADRDRF1AG077443 · NIA · STANFORD UNIVERSITY · PI AGHAEEPOUR, NIMA, MONTINE, THOMAS J · 2023 to 2023
$2.2M
Basal Ganglia Modulation of Cognitive Systems in Parkinson's diseaseK23NS075097 · NINDS · STANFORD UNIVERSITY · PI POSTON, KATHLEEN LOMBARD · 2011 to 2015
$936k
Neuropathology of synapses in AD and ADRDR01AG077443 · NIA · STANFORD UNIVERSITY · PI Nima Aghaeepour, Thomas J Montine · 2026 to 2026
$707k
The impact of early medial temporal lobe Tau in human cognitive agingR21AG058859 · NIA · STANFORD UNIVERSITY · PI MORMINO, ELIZABETH · 2018 to 2019
$432k
Regional tau deposition and digital assessment of cognition in preclinical AD and MCIK99AG071837 · NIA · STANFORD UNIVERSITY · PI YOUNG, CHRISTINA B · 2022 to 2023
$256k
Characterizing sleep-wake activity patterns to detect early Alzheimer's disease in normal older individualsF32AG074625 · NIA · STANFORD UNIVERSITY · PI WINER, JOSEPH ROBERT · 2021 to 2023
$207k
Alzheimer's Association AARFD-21-849349Michael J. Fox Foundation for Parkinson's Research 6440.0National Alzheimer's Coordinating Center P30-AG066515NIA NIH HHS AG047366NIA NIH HHS F32 AG074625NIA NIH HHS F32AG074625NIA NIH HHS K99 AG071837NIA NIH HHS P30 AG066515NIA NIH HHS P50 AG047366NIA NIH HHS R01 AG074339NIA NIH HHS R01 AG077443NIA NIH HHS R21 AG058859NIA NIH HHS R21AG058859NIA NIH HHS RF1 AG077443NIA NIH HHS RF1AG077443NIA NIH HHS U24 AG021886NIGMS NIH HHS K99AG071837NINDS NIH HHS K23 NS075097NINDS NIH HHS NS062684NINDS NIH HHS NS075097NINDS NIH HHS P50 NS062684NINDS NIH HHS R01 NS115114NINDS NIH HHS R01NS115114
6 · The paper itself

Abstract

objectiveTo determine whether plasma phosphorylated-Tau181 (pTau181) could be used as a diagnostic biomarker of concurrent Alzheimer's disease neuropathologic change (ADNC) or amyloidosis alone, as well as a prognostic, monitoring, and susceptibility/risk biomarker for clinical outcomes in Lewy body disease (LBD).

methodsWe studied 565 participants: 94 LBD with normal cognition, 83 LBD with abnormal cognition, 114 with Alzheimer's disease, and 274 cognitively normal. Plasma pTau181 levels were measured with the Lumipulse G platform. Diagnostic accuracy for concurrent ADNC and amyloidosis was assessed with Receiver Operating Characteristic curves in a subset of participants with CSF pTau181/Aβ42, and CSF Aβ42/Aβ40 or amyloid-β PET, respectively. Linear mixed effects models were used to examine the associations between baseline and longitudinal plasma pTau181 levels and clinical outcomes.

resultsPlasma pTau181 predicted concurrent ADNC and amyloidosis in LBD with abnormal cognition with 87% and 72% accuracy, respectively. In LBD patients with abnormal cognition, higher baseline plasma pTau181 was associated with worse baseline MoCA and CDR-SB, as well as accelerated decline in CDR-SB. Additionally, in this group, rapid increases in plasma pTau181 over 3 years predicted a faster decline in CDR-SB and memory. In LBD patients with normal cognition, there was no association between baseline or longitudinal plasma pTau181 levels and clinical outcomes; however, elevated pTau181 at baseline increased the risk of conversion to cognitive impairment.

interpretationOur findings suggest that plasma pTau181 is a promising biomarker for concurrent ADNC and amyloidosis in LBD. Furthermore, plasma pTau181 holds potential as a prognostic, monitoring, and susceptibility/risk biomarker, predicting disease progression in LBD. ANN NEUROL 2024;96:526-538.

Indexed as

Alzheimer DiseaseBiomarkersLewy Body Diseasetau ProteinsAgedAged, 80 and overAmyloid beta-PeptidesAmyloidosisCognitive DysfunctionFemaleHumansMaleMiddle AgedPhosphorylationPrognosisAmyloid beta-PeptidesBiomarkerstau Proteins

Identifiers

PMID38888142
PMCPMC11324388

What Socratic holds

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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 Socratic graph.