Evidence map›Paper›PMID 40047995›Full record

ArticleJournal of neurology2025

Tau levels in platelets isolated from Huntington's disease patients serve as a biomarker of disease severity.

Melanie Alpaugh, Juan Lantero-Rodriguez, Andrea L Benedet, Uriel Manseau, Martine Boutin, Massimo Maiuri, Helena L Denis, Maria Masnata, Shaline V Fazal, Sylvain Chouinard and 6 more

Abstract read
In one paragraph

Article in Journal of neurology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Stage-dependent tau-PET signatures in Huntington's disease revealed by [¹⁸F]PI-2620.European journal of nuclear medicine and molecular imaging · 2026
    Article
  2. Review
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

16 authors.

Melanie AlpaughDepartment of Molecular and Cellular Biology, University of Guelph, Guelph, Canada. alpaughm@uoguelph.ca.ORCID http://orcid.org/0000-0002-2782-5454
Juan Lantero-RodriguezInstitute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden.
Andrea L BenedetInstitute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden.
Uriel ManseauDepartment of Mathematical and Industrial Engineering, Polytechnique Montreal, Montreal, Canada.
Martine BoutinDépartement de Psychiatrie & Neurosciences, Faculté de Médecine, Université Laval, Quebec, Canada.
Massimo MaiuriDepartment of Molecular and Cellular Biology, University of Guelph, Guelph, Canada.
Helena L DenisDépartement de Psychiatrie & Neurosciences, Faculté de Médecine, Université Laval, Quebec, Canada.
Maria MasnataDépartement de Psychiatrie & Neurosciences, Faculté de Médecine, Université Laval, Quebec, Canada.
Shaline V FazalDepartment of Clinical Neurosciences, John Van Geest Centre for Brain Repair, University of Cambridge, Cambridge, UK.
Sylvain ChouinardDepartment of Movement Disorders, Centre Hospitalier Universitaire de Montréal-Hôtel Dieu, CHUM, Montréal, Canada.
Pedro Rosa-NetoTranslational Neuroimaging Laboratory, McGill University Research Centre for Studies in Aging, Douglas Research Institute, Le Centre Intégré Universitaire de Santé et de Services Sociaux (CIUSSS) de l'Ouest-de-L'Île-de-Montréal, Montreal, Canada.
Roger A BarkerDepartment of Clinical Neurosciences, John Van Geest Centre for Brain Repair, University of Cambridge, Cambridge, UK.
Kaj BlennowInstitute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden.
Henrik ZetterbergInstitute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden.
Richard LabibDepartment of Mathematical and Industrial Engineering, Polytechnique Montreal, Montreal, Canada.
Francesca CicchettiDépartement de Psychiatrie & Neurosciences, Faculté de Médecine, Université Laval, Quebec, Canada. francesca.cicchetti@crchudequebec.ulaval.ca.

Funding

Alzheimerfonden AF-930351Alzheimerfonden AF-939721Alzheimerfonden AF-968270Alzheimer's Association ADSF-21-831376-CAlzheimer's Association ADSF-21-831377-CAlzheimer's Association ADSF-21-831381-CAlzheimer's Association ADSF-24-1284328-CAlzheimer's Association SG-23-1038904 QCAlzheimer's Association ZEN-21-848495Alzheimer's Drug Discovery Foundation 201809-2016862EU Joint Programme - Neurodegenerative Disease Research JPND2019-466-236EU Joint Programme - Neurodegenerative Disease Research JPND2021-00694European Partnership on Metrology #22HLT07European Union's Horizon Europe research and innovation programme 101053962Hjärnfonden ALZ2022-0006Hjärnfonden FO2017-0243Hjärnfonden FO2022-0270HORIZON EUROPE Marie Sklodowska-Curie Actions 860197UK Dementia Research Institute UKDRI-1003Vetenskapsrådet 2017-00915Vetenskapsrådet 2019-02397Vetenskapsrådet 2022-00732Vetenskapsrådet 2022-01018Vetenskapsrådet 2023-00356Vetenskapsrådet ALFGBG-71320Vetenskapsrådet ALFGBG-715986Vetenskapsrådet ALFGBG-965240Wellcome Trust
6 · The paper itself

Abstract

Tau is a microtubule protein that is known to be hyperphosphorylated and to aggregate in several chronic neurodegenerative disorders. In many cases, in particular in Alzheimer's disease, the degree of tau pathology has been demonstrated to correlate with cognitive deficits and/or decline. In Huntington's disease (HD), a dominantly inherited neurodegenerative disorder, both cognitive impairments and abnormal tau expression have been reported to occur, along with the accumulation of the mutant huntingtin protein. In this respect, tau has been shown to be present in the cerebrospinal fluid of individuals with HD and to increase with disease progression. However, how this relates to changes in tau found in the periphery is largely unknown. In this study, we collected blood samples from patients with HD and isolated multiple blood components including plasma, platelets, and peripheral blood mononuclear cells to measure their tau levels and subsequently correlate these to cognitive impairments and disease stage. Our results suggest that the amount of tau, particularly N-terminal tau (NTA-tau) and total tau (t-tau), is elevated in all assayed blood components and that the quantity of tau within platelets, specifically, is strongly correlated with disease severity.

Indexed as

Blood PlateletsHuntington Diseasetau ProteinsAdultAgedBiomarkersFemaleHumansMaleMiddle AgedSeverity of Illness IndexBiomarkersMAPT protein, humantau ProteinsBloodCognitionNTA-tauPBMCPhosphorylated tauPlasma

Identifiers

PMID40047995
PMCPMC11885373

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.