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

Humans Lewy Body Disease / blood tau Proteins / blood Female Biomarkers / blood Male Aged Amyloid beta-Peptides / blood Retrospective Studies Alzheimer Disease / blood Middle Aged Aged, 80 and over Axons / pathology Neuroinflammatory Diseases / blood Chitinase-3-Like Protein 1 / blood Glial Fibrillary Acidic Protein / blood Neurofilament Proteins / blood Peptide Fragments / blood Receptors, Immunologic / blood Diagnosis, Differential Membrane Glycoproteins
Alzheimer’s disease Amyloid pathology Dementia with Lewy bodies Plasma biomarkers

Journal

Alzheimer's research & therapy
ISSN: 1758-9193
Titre abrégé: Alzheimers Res Ther
Pays: England
ID NLM: 101511643

Informations de publication

Date de publication:
03 Jul 2024
Historique:
received: 12 03 2024
accepted: 12 06 2024
medline: 4 7 2024
pubmed: 4 7 2024
entrez: 3 7 2024
Statut: epublish

Résumé

Increasing 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. We 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. DLB 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. Amyloid, 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.

Sections du résumé

BACKGROUND BACKGROUND
Increasing 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.
METHODS METHODS
We 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.
RESULTS RESULTS
DLB 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.
CONCLUSIONS CONCLUSIONS
Amyloid, 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.

Identifiants

DOI: 10.1186/s13195-024-01502-y PMID: 38961441
pubmed: 38961441
doi: 10.1186/s13195-024-01502-y
pii: 10.1186/s13195-024-01502-y
doi:

Substances chimiques

tau Proteins 0
Biomarkers 0
Amyloid beta-Peptides 0
Chitinase-3-Like Protein 1 0
Glial Fibrillary Acidic Protein 0
Neurofilament Proteins 0
TREM2 protein, human 0
CHI3L1 protein, human 0
Peptide Fragments 0
neurofilament protein L 0
GFAP protein, human 0
Receptors, Immunologic 0
MAPT protein, human 0
Membrane Glycoproteins 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

146

Informations de copyright

© 2024. The Author(s).

Références

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Auteurs

Agathe Vrillon (A)

AP-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.
Université Paris Cité, INSERM, UMRS 1144, Paris, France. agathe.vrillon@aphp.fr.
University of California San Francisco, San Francisco, USA. agathe.vrillon@aphp.fr.

Olivier Bousiges (O)

Laboratory of Biochemistry and Molecular Biology, University Hospital of Strasbourg, Strasbourg, France.
University of Strasbourg and CNRS, ICube laboratory UMR 7357 and FMTS (Fédération de Médecine Translationnelle de Strasbourg), team IMIS Strasbourg, Strasbourg, France.

Karl Götze (K)

Université Paris Cité, INSERM, UMRS 1144, Paris, France.

Catherine Demuynck (C)

CM2R (Memory Resource and Research Centre), Service of Gerontology Mobile-Neuro-Psy-Research, Geriatrics Department, University Hospital of Strasbourg, Strasbourg, France.

Candice Muller (C)

CM2R (Memory Resource and Research Centre), Service of Gerontology Mobile-Neuro-Psy-Research, Geriatrics Department, University Hospital of Strasbourg, Strasbourg, France.

Alix Ravier (A)

CM2R (Memory Resource and Research Centre), Service of Gerontology Mobile-Neuro-Psy-Research, Geriatrics Department, University Hospital of Strasbourg, Strasbourg, France.

Benoît Schorr (B)

CM2R (Memory Resource and Research Centre), Service of Gerontology Mobile-Neuro-Psy-Research, Geriatrics Department, University Hospital of Strasbourg, Strasbourg, France.

Nathalie Philippi (N)

University of Strasbourg and CNRS, ICube laboratory UMR 7357 and FMTS (Fédération de Médecine Translationnelle de Strasbourg), team IMIS Strasbourg, Strasbourg, France.
CM2R (Memory Resource and Research Centre), Service of Gerontology Mobile-Neuro-Psy-Research, Geriatrics Department, University Hospital of Strasbourg, Strasbourg, France.
Neuropsychology unit, Service of Neurology Strasbourg, University Hospital of Strasbourg, Strasbourg, France.

Claire Hourregue (C)

AP-HP Nord, Cognitive Neurology Center Hôpital Lariboisière-Fernand Widal, Université Paris Cité, 200 rue du Faubourg Saint-Denis, Paris, 75010, France.

Emmanuel Cognat (E)

AP-HP Nord, Cognitive Neurology Center Hôpital Lariboisière-Fernand Widal, Université Paris Cité, 200 rue du Faubourg Saint-Denis, Paris, 75010, France.
Université Paris Cité, INSERM, UMRS 1144, Paris, France.

Julien Dumurgier (J)

AP-HP Nord, Cognitive Neurology Center Hôpital Lariboisière-Fernand Widal, Université Paris Cité, 200 rue du Faubourg Saint-Denis, Paris, 75010, France.

Matthieu Lilamand (M)

AP-HP Nord, Cognitive Neurology Center Hôpital Lariboisière-Fernand Widal, Université Paris Cité, 200 rue du Faubourg Saint-Denis, Paris, 75010, France.

Benjamin Cretin (B)

University of Strasbourg and CNRS, ICube laboratory UMR 7357 and FMTS (Fédération de Médecine Translationnelle de Strasbourg), team IMIS Strasbourg, Strasbourg, France.
CM2R (Memory Resource and Research Centre), Service of Gerontology Mobile-Neuro-Psy-Research, Geriatrics Department, University Hospital of Strasbourg, Strasbourg, France.
Neuropsychology unit, Service of Neurology Strasbourg, University Hospital of Strasbourg, Strasbourg, France.

Frédéric Blanc (F)

University of Strasbourg and CNRS, ICube laboratory UMR 7357 and FMTS (Fédération de Médecine Translationnelle de Strasbourg), team IMIS Strasbourg, Strasbourg, France.
CM2R (Memory Resource and Research Centre), Service of Gerontology Mobile-Neuro-Psy-Research, Geriatrics Department, University Hospital of Strasbourg, Strasbourg, France.
Neuropsychology unit, Service of Neurology Strasbourg, University Hospital of Strasbourg, Strasbourg, France.

Claire Paquet (C)

AP-HP Nord, Cognitive Neurology Center Hôpital Lariboisière-Fernand Widal, Université Paris Cité, 200 rue du Faubourg Saint-Denis, Paris, 75010, France.
Université Paris Cité, INSERM, UMRS 1144, Paris, France.

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