Evidence map›Paper›PMID 33585983›Full record

ArticleActa neuropathologica2021

Plasma p-tau231: a new biomarker for incipient Alzheimer's disease pathology.

Nicholas J Ashton, Tharick A Pascoal, Thomas K Karikari, Andréa L Benedet, Juan Lantero-Rodriguez, Gunnar Brinkmalm, Anniina Snellman, Michael Schöll, Claire Troakes, Abdul Hye and 5 more

2 registry-linked trialsAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Acta neuropathologica, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 422 papers, 8 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
422citing papers in PubMed, 8 pooled it
–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.

NCT06072963 phase2recruitingstarted 2024, after this paper: background citation

Combination of Intranasal Insulin With Oral Semaglutide to Improve Cognition and Cerebral Blood Flow: a Feasibility Study

Ran2024Enrolled80Registered outcomes15Posted comparisons0ConditionsAlzheimer Disease, Metabolic Syndrome, Mild Cognitive ImpairmentArmsIntranasal insulin, Intranasal insulin placebo, semaglutide, Semaglutide placebo
PMID 36871874PMID 29687620PMID 32296731PMID 19237574PMID 21911655PMID 22015237PMID 23332364PMID 23687103PMID 25150735PMID 26711459PMID 27255817PMID 27350397other papers from this trial
Open the trial in the graph
NCT06529744 recruitingnot on this mapstarted 2023, after this paper: background citation

Improving Prognostic Confidence in Neurodegenerative Diseases Causing Dementia Using Peripheral Biomarkers and Integrative Modeling

Typeobservational_patient_registrySponsorUniversity Health Network, TorontoRan2023 to 2027Enrolled500ConditionsDementia, Alzheimer Disease, Dementia With Lewy Bodies, Vascular Dementia
3 · Its place in the literature

Who cites it

422 citing papers in PubMed, 8 syntheses or guidelines pooled it.

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  16. Investigating AD and non-AD [European journal of nuclear medicine and molecular imaging · 2026
    Article
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362 more citing papers are in PubMed but not listed here.

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

15 authors.

Nicholas J Ashton *Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden. nicholas.ashton@gu.se.ORCID http://orcid.org/0000-0002-6353-9316
Tharick A Pascoal *Translational Neuroimaging Laboratory, McGill Centre for Studies in Aging, McGill University, Montreal, QC, Canada.
Thomas K KarikariDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Andréa L BenedetDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Juan Lantero-RodriguezDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Gunnar BrinkmalmDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Anniina SnellmanDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Michael SchöllDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Claire TroakesDepartment of Basic and Clinical Neuroscience, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.
Abdul HyeKing's College London, Institute of Psychiatry, Psychology and Neuroscience, Maurice Wohl Institute Clinical Neuroscience Institute, London, UK.
Serge GauthierAlzheimer's Disease Research Unit, The McGill University Research Centre for Studies in Aging, Montreal, McGill University, Montreal, QC, Canada.
Eugeen VanmechelenADx NeuroSciences, Technologiepark 94, 9052, Ghent, Belgium.
Henrik ZetterbergDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Pedro Rosa-Neto *Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Kaj Blennow *Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden. kaj.blennow@neuro.gu.se.

Funding

CIHR MOP-11–51-31Medical Research Council MR/L016397/1
6 · The paper itself

Abstract

The quantification of phosphorylated tau in biofluids, either cerebrospinal fluid (CSF) or plasma, has shown great promise in detecting Alzheimer's disease (AD) pathophysiology. Tau phosphorylated at threonine 231 (p-tau231) is one such biomarker in CSF but its usefulness as a blood biomarker is currently unknown. Here, we developed an ultrasensitive Single molecule array (Simoa) for the quantification of plasma p-tau231 which was validated in four independent cohorts (n = 588) in different settings, including the full AD continuum and non-AD neurodegenerative disorders. Plasma p-tau231 was able to identify patients with AD and differentiate them from amyloid-β negative cognitively unimpaired (CU) older adults with high accuracy (AUC = 0.92-0.94). Plasma p-tau231 also distinguished AD patients from patients with non-AD neurodegenerative disorders (AUC = 0.93), as well as from amyloid-β negative MCI patients (AUC = 0.89). In a neuropathology cohort, plasma p-tau231 in samples taken on avergae 4.2 years prior to post-mortem very accurately identified AD neuropathology in comparison to non-AD neurodegenerative disorders (AUC = 0.99), this is despite all patients being given an AD dementia diagnosis during life. Plasma p-tau231 was highly correlated with CSF p-tau231, tau pathology as assessed by [

Indexed as

AgedAged, 80 and overAlzheimer DiseaseBiomarkersFemaleHumansMaleMiddle AgedPhosphorylationtau ProteinsBiomarkersMAPT protein, humantau ProteinsAlzheimer’s diseaseBiomarkersBloodBraakPreclinicalp-tau181p-tau217p-tau231Tau

Identifiers

PMID33585983
PMCPMC8043944

What OpenQuestion holds

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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.