Evidence map›Paper›PMID 32674011›Full record

ArticleNeuroImage. Clinical2020

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

Carla Abdelnour, Daniel Ferreira, Ketil Oppedal, Lena Cavallin, Olivier Bousiges, Lars Olof Wahlund, Jakub Hort, Zuzana Nedelska, Alessandro Padovani, Andrea Pilotto and 8 more

Open access · goldAbstract read
In one paragraph

Article in NeuroImage. Clinical, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 6% of its field
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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Sex differences inFrontiers in dementia · 2025
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  15. Sex differences in brain atrophy in dementia with Lewy bodies.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
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  19. Dementia with Lewy bodies: Impact of co-pathologies and implications for clinical trial design.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023
    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

18 authors at 15 institutions in 8 countries.

Carla AbdelnourResearch 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 FerreiraDivision of Clinical Geriatrics, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden.
Ketil OppedalCentre 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 CavallinDepartment of Neuroscience, Karolinska Institutet and Department of Radiology Karolinska University Hospital, Stockholm, Sweden.
Olivier BousigesHôpitaux Universitaire de Strasbourg, Laboratoire de Biochimie et Biologie Moléculaire, et CNRS, Laboratoire de Neurosciences Cognitives et Adaptatives (LNCA), UMR7364, Strasbourg, France.
Lars Olof WahlundDivision of Clinical Geriatrics, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden.
Jakub HortDepartment of Neurology, Charles University, 2nd Medical Faculty and Motol University Hospital, Prague, Czech Republic; International Clinical Research Centre, Brno, Czech Republic.
Zuzana NedelskaDepartment of Neurology, Charles University, 2nd Medical Faculty and Motol University Hospital, Prague, Czech Republic; International Clinical Research Centre, Brno, Czech Republic.
Alessandro PadovaniNeurology Unit, Department of Clinical and Experimental Sciences, University of Brescia, Brescia, Italy.
Andrea PilottoNeurology Unit, Department of Clinical and Experimental Sciences, University of Brescia, Brescia, Italy.
Laura BonanniDepartment of Neuroscience Imaging and Clinical Sciences and CESI, University G d'Annunzio of Chieti-Pescara, Chieti, Italy.
Milica G KrambergerDepartment of Neurology, University Medical Centre Ljubljana, Medical faculty, University of Ljubljana, Ljubljana, Slovenia.
Mercè BoadaResearch 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 WestmanDivision 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 PagonabarragaMovement 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 KulisevskyMovement 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 BlancHôpitaux 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 AarslandCentre for Age-Related Medicine, Stavanger University Hospital, Stavanger, Norway; Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.
Biomedical Research Networking Center on Neurodegenerative Diseases · ESKarolinska Institutet · SEUniversity of Brescia · ITCharles University · CZFundació ACE · ESHôpitaux Universitaires de Strasbourg · FRInternational Clinical Research Center, St. Anne's University Hospital Brno · CZKarolinska University Hospital · SELaboratoire de Neurosciences Cognitives · FRLjubljana University Medical Centre · SIStavanger University Hospital · NOUniversitat Autònoma de Barcelona · ESUniversity of Chieti-Pescara · ITUniversity of Stavanger · NOWellcome Centre for Human Neuroimaging · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlzheimer'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.

objectivesWe 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.

methods86 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.

resultsDLB 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.

conclusionsThis 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.

Indexed as

Alzheimer DiseaseLewy Body DiseaseAgedAmyloid beta-PeptidesAtrophyBiomarkersBrainHumansMalePeptide Fragmentstau ProteinsAmyloid beta-PeptidesBiomarkersPeptide Fragmentstau ProteinsAlzheimer diseaseAtrophyBiomarkersLewy body diseaseNeuroimaging

Identifiers

PMID32674011
PMCPMC7363702
OpenAlexW3039659171

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.