The combined effect of amyloid-β and tau biomarkers on brain atrophy in dementia with Lewy bodies.

Aged Alzheimer Disease / diagnostic imaging Amyloid beta-Peptides Atrophy Biomarkers Brain / diagnostic imaging Humans Lewy Body Disease / diagnostic imaging Male Peptide Fragments tau Proteins
Alzheimer disease Atrophy Biomarkers Lewy body disease Neuroimaging

Journal

NeuroImage. Clinical
ISSN: 2213-1582
Titre abrégé: Neuroimage Clin
Pays: Netherlands
ID NLM: 101597070

Informations de publication

Date de publication:
2020
Historique:
received: 01 03 2020
revised: 05 06 2020
accepted: 26 06 2020
pubmed: 17 7 2020
medline: 29 6 2021
entrez: 17 7 2020
Statut: ppublish

Résumé

Alzheimer's disease (AD)-related pathology is frequently found in patients with dementia with Lewy bodies (DLB). However, it is unknown how amyloid-β and tau-related pathologies influence neurodegeneration in DLB. Understanding the mechanisms underlying brain atrophy in DLB can improve our knowledge about disease progression, differential diagnosis, drug development and testing of anti-amyloid and anti-tau therapies in DLB. We aimed at investigating the combined effect of CSF amyloid-β42, phosphorylated tau and total tau on regional brain atrophy in DLB in the European DLB (E-DLB) cohort. 86 probable DLB patients from the E-DLB cohort with CSF and MRI data were included. Random forest was used to analyze the association of CSF biomarkers (predictors) with visual rating scales for medial temporal lobe atrophy (MTA), posterior atrophy (PA) and global cortical atrophy scale-frontal subscale (GCA-F) (outcomes), including age, sex, education and disease duration as extra predictors. DLB patients with abnormal MTA scores had abnormal CSF Aβ42, shorter disease duration and older age. DLB patients with abnormal PA scores had abnormal levels of CSF Aβ42 and p-tau, older age, lower education and shorter disease duration. Abnormal GCA-F scores were associated with lower education, male sex, and older age, but not with any AD-related CSF biomarker. This study shows preliminary data on the potential combined effect of amyloid-β and tau-related pathologies on the integrity of posterior brain cortices in DLB patients, whereas only amyloid-β seems to be related to MTA. Future availability of α-synuclein biomarkers will help us to understand the effect of α-synuclein and AD-related pathologies on brain integrity in DLB.

Sections du résumé

BACKGROUND
Alzheimer's disease (AD)-related pathology is frequently found in patients with dementia with Lewy bodies (DLB). However, it is unknown how amyloid-β and tau-related pathologies influence neurodegeneration in DLB. Understanding the mechanisms underlying brain atrophy in DLB can improve our knowledge about disease progression, differential diagnosis, drug development and testing of anti-amyloid and anti-tau therapies in DLB.
OBJECTIVES
We aimed at investigating the combined effect of CSF amyloid-β42, phosphorylated tau and total tau on regional brain atrophy in DLB in the European DLB (E-DLB) cohort.
METHODS
86 probable DLB patients from the E-DLB cohort with CSF and MRI data were included. Random forest was used to analyze the association of CSF biomarkers (predictors) with visual rating scales for medial temporal lobe atrophy (MTA), posterior atrophy (PA) and global cortical atrophy scale-frontal subscale (GCA-F) (outcomes), including age, sex, education and disease duration as extra predictors.
RESULTS
DLB patients with abnormal MTA scores had abnormal CSF Aβ42, shorter disease duration and older age. DLB patients with abnormal PA scores had abnormal levels of CSF Aβ42 and p-tau, older age, lower education and shorter disease duration. Abnormal GCA-F scores were associated with lower education, male sex, and older age, but not with any AD-related CSF biomarker.
CONCLUSIONS
This study shows preliminary data on the potential combined effect of amyloid-β and tau-related pathologies on the integrity of posterior brain cortices in DLB patients, whereas only amyloid-β seems to be related to MTA. Future availability of α-synuclein biomarkers will help us to understand the effect of α-synuclein and AD-related pathologies on brain integrity in DLB.

Identifiants

DOI: 10.1016/j.nicl.2020.102333 PMID: 32674011 PMC: PMC7363702
pubmed: 32674011
pii: S2213-1582(20)30170-4
doi: 10.1016/j.nicl.2020.102333
pmc: PMC7363702
pii:
doi:

Substances chimiques

Amyloid beta-Peptides 0
Biomarkers 0
Peptide Fragments 0
tau Proteins 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

102333

Informations de copyright

Copyright © 2020 The Authors. Published by Elsevier Inc. All rights reserved.

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Auteurs

Carla Abdelnour (C)

Research Center and Memory Clinic, Fundació ACE, Institut Català de Neurociències Aplicades, Universitat Internacional de Catalunya-Barcelona, Centro de Investigación en Red-Enfermedades Neurodegenerativas (CIBERNED), Barcelona, Spain; Department of Medicine of the Universitat Autònoma de Barcelona, Barcelona, Spain. Electronic address: cabdelnour@fundacioace.org.

Daniel Ferreira (D)

Division of Clinical Geriatrics, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden.

Ketil Oppedal (K)

Centre for Age-Related Medicine, Stavanger University Hospital, Stavanger, Norway; Department of Radiology, Stavanger University Hospital, Stavanger, Norway; Department of Electrical Engineering and Computer Science, University of Stavanger, Stavanger, Norway.

Lena Cavallin (L)

Department of Neuroscience, Karolinska Institutet and Department of Radiology Karolinska University Hospital, Stockholm, Sweden.

Olivier Bousiges (O)

Hôpitaux Universitaire de Strasbourg, Laboratoire de Biochimie et Biologie Moléculaire, et CNRS, Laboratoire de Neurosciences Cognitives et Adaptatives (LNCA), UMR7364, Strasbourg, France.

Lars Olof Wahlund (LO)

Division of Clinical Geriatrics, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden.

Jakub Hort (J)

Department of Neurology, Charles University, 2nd Medical Faculty and Motol University Hospital, Prague, Czech Republic; International Clinical Research Centre, Brno, Czech Republic.

Zuzana Nedelska (Z)

Department of Neurology, Charles University, 2nd Medical Faculty and Motol University Hospital, Prague, Czech Republic; International Clinical Research Centre, Brno, Czech Republic.

Alessandro Padovani (A)

Neurology Unit, Department of Clinical and Experimental Sciences, University of Brescia, Brescia, Italy.

Andrea Pilotto (A)

Neurology Unit, Department of Clinical and Experimental Sciences, University of Brescia, Brescia, Italy.

Laura Bonanni (L)

Department of Neuroscience Imaging and Clinical Sciences and CESI, University G d'Annunzio of Chieti-Pescara, Chieti, Italy.

Milica G Kramberger (MG)

Department of Neurology, University Medical Centre Ljubljana, Medical faculty, University of Ljubljana, Ljubljana, Slovenia.

Mercè Boada (M)

Research Center and Memory Clinic, Fundació ACE, Institut Català de Neurociències Aplicades, Universitat Internacional de Catalunya-Barcelona, Centro de Investigación en Red-Enfermedades Neurodegenerativas (CIBERNED), Barcelona, Spain.

Eric Westman (E)

Division of Clinical Geriatrics, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden; Department of Neuroimaging, Centre for Neuroimaging Sciences, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.

Javier Pagonabarraga (J)

Movement Disorders Unit, Neurology Department, Hospital de la Santa Creu i Sant Pau. Biomedical Research Institute (IIB-Sant Pau), Centro de Investigación en Red-Enfermedades Neurodegenerativas (CIBERNED), Barcelona, Spain.

Jaime Kulisevsky (J)

Movement Disorders Unit, Neurology Department, Hospital de la Santa Creu i Sant Pau. Biomedical Research Institute (IIB-Sant Pau), Centro de Investigación en Red-Enfermedades Neurodegenerativas (CIBERNED), Barcelona, Spain.

Frédéric Blanc (F)

Hôpitaux Universitaire de Strasbourg, CMRR (Centre Mémoire de Ressource et de Recherche), Hôpital de jour, pôle de Gériatrie, et CNRS, laboratoire ICube UMR 7357 et FMTS (Fédération de MédecineTranslationnelle de Strasbourg), équipe IMIS/Neurocrypto, Strasbourg, France.

Dag Aarsland (D)

Centre for Age-Related Medicine, Stavanger University Hospital, Stavanger, Norway; Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.

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Classifications MeSH

questionsmedicales.fr › Personnes › Tranches d'âge › Adulte › Sujet âgé › The combined effect of amyloid-β and tau...
questionsmedicales.fr › Troubles mentaux › Troubles neurocognitifs › Démence › Maladie d'Alzheimer › The combined effect of amyloid-β and tau...
questionsmedicales.fr › Acides aminés, peptides et protéines › Protéines › Protéines membranaires › Peptides bêta-amyloïdes › The combined effect of amyloid-β and tau...
questionsmedicales.fr › États, signes et symptômes pathologiques › États anatomopathologiques › Atrophie › The combined effect of amyloid-β and tau...
questionsmedicales.fr › Facteurs biologiques › Marqueurs biologiques › The combined effect of amyloid-β and tau...
questionsmedicales.fr › Système nerveux › Système nerveux central › Encéphale › The combined effect of amyloid-β and tau...
questionsmedicales.fr › Eucaryotes › Animaux › Chordés › Vertébrés › Mammifères › Eutheria › Primates › Haplorhini › Catarrhini › Hominidae › Humains › The combined effect of amyloid-β and tau...
questionsmedicales.fr › Troubles mentaux › Troubles neurocognitifs › Démence › Maladie à corps de Lewy › The combined effect of amyloid-β and tau...
questionsmedicales.fr › Acides aminés, peptides et protéines › Peptides › Fragments peptidiques › The combined effect of amyloid-β and tau...
questionsmedicales.fr › Acides aminés, peptides et protéines › Protéines › Protéines de tissu nerveux › Protéines associées aux microtubules › Protéines tau › The combined effect of amyloid-β and tau...