Evidence map›Paper›PMID 33008460›Full record

ArticleAlzheimer's research & therapy2020

Cerebrospinal fluid A beta 1-40 peptides increase in Alzheimer's disease and are highly correlated with phospho-tau in control individuals.

Sylvain Lehmann, Julien Dumurgier, Xavier Ayrignac, Cecilia Marelli, Daniel Alcolea, Juan Fortea Ormaechea, Eric Thouvenot, Constance Delaby, Christophe Hirtz, Jérôme Vialaret and 8 more

Open access · goldAbstract readMulticenter Study
In one paragraph

Article in Alzheimer's research & therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

34 citing papers in PubMed, 65 citations in OpenAlex.

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  13. sPDGFRβ and neuroinflammation are associated with AD biomarkers and differ by race: The ASCEND Study.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
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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 2 institutions in 2 countries.

Sylvain LehmannUniv Montpellier, CHU Montpellier (LBPC-PPC), INSERM (IRMB, INM), Montpellier, France. s-lehmann@chu-montpellier.fr.ORCID 0000-0001-6117-562X
Julien DumurgierCentre de Neurologie Cognitive et Service de Biochimie et de Biologie Moléculaire, Groupe Hospitalier Lariboisière Fernand-Widal, INSERMU942, Université Paris Diderot, Paris, France.
Xavier AyrignacCHU de Montpellier, Département de Neurologie, INSERM, Univ Montpellier, Montpellier, France.
Cecilia MarelliCHU de Montpellier, Département de Neurologie, INSERM, Univ Montpellier, Montpellier, France.
Daniel AlcoleaSant Pau Memory Unit, Department of Neurology, Universitat Autònoma de Barcelona, Barcelona, Spain.
Juan Fortea OrmaecheaSant Pau Memory Unit, Department of Neurology, Universitat Autònoma de Barcelona, Barcelona, Spain.
Eric ThouvenotCHU de Nîmes, Département de Neurologie, INSERM, Univ Montpellier, Montpellier, France.
Constance DelabyUniv Montpellier, CHU Montpellier (LBPC-PPC), INSERM (IRMB, INM), Montpellier, France.
Christophe HirtzUniv Montpellier, CHU Montpellier (LBPC-PPC), INSERM (IRMB, INM), Montpellier, France.
Jérôme VialaretUniv Montpellier, CHU Montpellier (LBPC-PPC), INSERM (IRMB, INM), Montpellier, France.
Nelly GinestetUniv Montpellier, CHU Montpellier (LBPC-PPC), INSERM (IRMB, INM), Montpellier, France.
Elodie Bouaziz-AmarCentre de Neurologie Cognitive et Service de Biochimie et de Biologie Moléculaire, Groupe Hospitalier Lariboisière Fernand-Widal, INSERMU942, Université Paris Diderot, Paris, France.
Jean-Louis LaplancheCentre de Neurologie Cognitive et Service de Biochimie et de Biologie Moléculaire, Groupe Hospitalier Lariboisière Fernand-Widal, INSERMU942, Université Paris Diderot, Paris, France.
Pierre LabaugeCHU de Montpellier, Département de Neurologie, INSERM, Univ Montpellier, Montpellier, France.
Claire PaquetCentre de Neurologie Cognitive et Service de Biochimie et de Biologie Moléculaire, Groupe Hospitalier Lariboisière Fernand-Widal, INSERMU942, Université Paris Diderot, Paris, France.
Alberto LleoSant Pau Memory Unit, Department of Neurology, Universitat Autònoma de Barcelona, Barcelona, Spain.
Audrey GabelleUniv Montpellier, INSERM, CHU Montpellier (CMRR), Montpellier, France.
Alzheimer’s Disease Neuroimaging Initiative (ADNI)
Inserm · FRUniversitat Autònoma de Barcelona · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAmyloid pathology, which is one of the characteristics of Alzheimer's disease (AD), results from altered metabolism of the beta-amyloid (Aβ) peptide in terms of synthesis, clearance, or aggregation. A decrease in cerebrospinal fluid (CSF) level Aβ1-42 is evident in AD, and the CSF ratio Aβ42/Aβ40 has recently been identified as one of the most reliable diagnostic biomarkers of amyloid pathology. Variations in inter-individual levels of Aβ1-40 in the CSF have been observed in the past, but their origins remain unclear. In addition, the variation of Aβ40 in the context of AD studied in several studies has yielded conflicting results.

methodsHere, we analyzed the levels of Aβ1-40 using multicenter data obtained on 2466 samples from six different cohorts in which CSF was collected under standardized protocols, centrifugation, and storage conditions. Tau and p-tau (181) concentrations were measured using commercially available in vitro diagnostic immunoassays. Concentrations of CSF Aβ1-42 and Aβ1-40 were measured by ELISA, xMAP technology, chemiluminescence immunoassay (CLIA), and mass spectrometry. Statistical analyses were calculated for parametric and non-parametric comparisons, linear regression, correlation, and odds ratios. The statistical tests were adjusted for the effects of covariates (age, in particular).

resultsRegardless of the analysis method used and the cohorts, a slight but significant age-independent increase in the levels of Aβ40 in CSF was observed in AD. We also found a strong positive correlation between the levels of Aβ1-40 and p-tau (181) in CSF, particularly in control patients.

conclusionsThese results indicate that an increase in the baseline level of amyloid peptides, which are associated with an increase in p-tau (181), may be a biological characteristic and possibly a risk factor for AD. Further studies will be needed to establish a causal link between increased baseline levels of Aβ40 and the development of the disease.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesBiomarkersHumansPeptide Fragmentstau ProteinsAmyloid beta-Peptidesamyloid beta-protein (1-40)BiomarkersPeptide Fragmentstau ProteinsAlzheimer’s diseaseAmyloid peptidesBiomarkersCerebrospinal fluid (CSF)Tau proteins

Identifiers

PMID33008460
PMCPMC7532565
OpenAlexW3091323015

What OpenQuestion holds

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Registered trials

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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.