Evidence map›Paper›PMID 38961441›Full record

ArticleAlzheimer's research & therapy2024

Plasma biomarkers of amyloid, tau, axonal, and neuroinflammation pathologies in dementia with Lewy bodies.

Agathe Vrillon, Olivier Bousiges, Karl Götze, Catherine Demuynck, Candice Muller, Alix Ravier, Benoît Schorr, Nathalie Philippi, Claire Hourregue, Emmanuel Cognat and 5 more

Abstract read
In one paragraph

Article in Alzheimer's research & therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 2 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.

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

22 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
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  11. Heterogeneity of dementia with lewy bodies: Insights from clinical presentations, neuropathology, and biomarkers.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025
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  17. Unravelling the plasma proteome: Pioneering biomarkers for differential dementia diagnosis.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  18. Article
  19. A hypothesis explaining Alzheimer's disease, Parkinson's disease, and dementia with Lewy bodies overlap.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Review
  20. 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

15 authors.

Agathe VrillonAP-HP Nord, Cognitive Neurology Center Hôpital Lariboisière-Fernand Widal, Université Paris Cité, 200 rue du Faubourg Saint-Denis, Paris, 75010, France. agathe.vrillon@aphp.fr.
Olivier BousigesLaboratory of Biochemistry and Molecular Biology, University Hospital of Strasbourg, Strasbourg, France.
Karl GötzeUniversité Paris Cité, INSERM, UMRS 1144, Paris, France.
Catherine DemuynckCM2R (Memory Resource and Research Centre), Service of Gerontology Mobile-Neuro-Psy-Research, Geriatrics Department, University Hospital of Strasbourg, Strasbourg, France.
Candice MullerCM2R (Memory Resource and Research Centre), Service of Gerontology Mobile-Neuro-Psy-Research, Geriatrics Department, University Hospital of Strasbourg, Strasbourg, France.
Alix RavierCM2R (Memory Resource and Research Centre), Service of Gerontology Mobile-Neuro-Psy-Research, Geriatrics Department, University Hospital of Strasbourg, Strasbourg, France.
Benoît SchorrCM2R (Memory Resource and Research Centre), Service of Gerontology Mobile-Neuro-Psy-Research, Geriatrics Department, University Hospital of Strasbourg, Strasbourg, France.
Nathalie PhilippiUniversity of Strasbourg and CNRS, ICube laboratory UMR 7357 and FMTS (Fédération de Médecine Translationnelle de Strasbourg), team IMIS Strasbourg, Strasbourg, France.
Claire HourregueAP-HP Nord, Cognitive Neurology Center Hôpital Lariboisière-Fernand Widal, Université Paris Cité, 200 rue du Faubourg Saint-Denis, Paris, 75010, France.
Emmanuel CognatAP-HP Nord, Cognitive Neurology Center Hôpital Lariboisière-Fernand Widal, Université Paris Cité, 200 rue du Faubourg Saint-Denis, Paris, 75010, France.
Julien DumurgierAP-HP Nord, Cognitive Neurology Center Hôpital Lariboisière-Fernand Widal, Université Paris Cité, 200 rue du Faubourg Saint-Denis, Paris, 75010, France.
Matthieu LilamandAP-HP Nord, Cognitive Neurology Center Hôpital Lariboisière-Fernand Widal, Université Paris Cité, 200 rue du Faubourg Saint-Denis, Paris, 75010, France.
Benjamin CretinUniversity of Strasbourg and CNRS, ICube laboratory UMR 7357 and FMTS (Fédération de Médecine Translationnelle de Strasbourg), team IMIS Strasbourg, Strasbourg, France.
Frédéric BlancUniversity of Strasbourg and CNRS, ICube laboratory UMR 7357 and FMTS (Fédération de Médecine Translationnelle de Strasbourg), team IMIS Strasbourg, Strasbourg, France.
Claire PaquetAP-HP Nord, Cognitive Neurology Center Hôpital Lariboisière-Fernand Widal, Université Paris Cité, 200 rue du Faubourg Saint-Denis, Paris, 75010, France.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIncreasing evidence supports the use of plasma biomarkers of amyloid, tau, neurodegeneration, and neuroinflammation for diagnosis of dementia. However, their performance for positive and differential diagnosis of dementia with Lewy bodies (DLB) in clinical settings is still uncertain.

methodsWe conducted a retrospective biomarker study in two tertiary memory centers, Paris Lariboisière and CM2RR Strasbourg, France, enrolling patients with DLB (n = 104), Alzheimer's disease (AD, n = 76), and neurological controls (NC, n = 27). Measured biomarkers included plasma Aβ40/Aβ42 ratio, p-tau181, NfL, and GFAP using SIMOA and plasma YKL-40 and sTREM2 using ELISA. DLB patients with available CSF analysis (n = 90) were stratified according to their CSF Aβ profile.

resultsDLB patients displayed modified plasma Aβ ratio, p-tau181, and GFAP levels compared with NC and modified plasma Aβ ratio, p-tau181, GFAP, NfL, and sTREM2 levels compared with AD patients. Plasma p-tau181 best differentiated DLB from AD patients (ROC analysis, area under the curve [AUC] = 0.80) and NC (AUC = 0.78), and combining biomarkers did not improve diagnosis performance. Plasma p-tau181 was the best standalone biomarker to differentiate amyloid-positive from amyloid-negative DLB cases (AUC = 0.75) and was associated with cognitive status in the DLB group. Combining plasma Aβ ratio, p-tau181 and NfL increased performance to identify amyloid copathology (AUC = 0.79). Principal component analysis identified different segregation patterns of biomarkers in the DLB and AD groups.

conclusionsAmyloid, tau, neurodegeneration and neuroinflammation plasma biomarkers are modified in DLB, albeit with moderate diagnosis performance. Plasma p-tau181 can contribute to identify Aβ copathology in DLB.

Indexed as

Amyloid beta-PeptidesBiomarkersLewy Body Diseasetau ProteinsAgedAged, 80 and overAlzheimer DiseaseAxonsChitinase-3-Like Protein 1Diagnosis, DifferentialFemaleGlial Fibrillary Acidic ProteinHumansMaleMembrane GlycoproteinsMiddle AgedAmyloid beta-PeptidesBiomarkersCHI3L1 protein, humanChitinase-3-Like Protein 1GFAP protein, humanGlial Fibrillary Acidic ProteinMAPT protein, humanMembrane Glycoproteinsneurofilament protein LNeurofilament ProteinsPeptide FragmentsReceptors, Immunologictau ProteinsTREM2 protein, humanAlzheimer’s diseaseAmyloid pathologyDementia with Lewy bodiesPlasma biomarkers

Identifiers

PMID38961441
PMCPMC11221164

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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.