Evidence map›Paper›PMID 31787105›Full record

ArticleAlzheimer's research & therapy2019

Plasma Aβ42/40 ratio alone or combined with FDG-PET can accurately predict amyloid-PET positivity: a cross-sectional analysis from the AB255 Study.

Virginia Pérez-Grijalba, Javier Arbizu, Judith Romero, Elena Prieto, Pedro Pesini, Leticia Sarasa, Fernando Guillen, Inmaculada Monleón, Itziar San-José, Pablo Martínez-Lage and 10 more

Open access · goldAbstract readMulticenter Study
In one paragraph

Article in Alzheimer's research & therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
4.9field-weighted citation impact, top 4% 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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.

  1. Pooled it
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  7. Nuclear medicine and molecular imaging · 2025
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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

20 authors at 4 institutions in 1 country.

Virginia Pérez-GrijalbaAraclon Biotech S.L., Vía Hispanidad 21, 50009, Zaragoza, Spain.
Javier ArbizuServicio de Medicina Nuclear, Clínica Universidad de Navarra, Pamplona, Spain.
Judith RomeroAraclon Biotech S.L., Vía Hispanidad 21, 50009, Zaragoza, Spain.
Elena PrietoServicio de Medicina Nuclear, Clínica Universidad de Navarra, Pamplona, Spain.
Pedro PesiniAraclon Biotech S.L., Vía Hispanidad 21, 50009, Zaragoza, Spain. ppesini@araclon.com.ORCID 0000-0002-0656-2384
Leticia SarasaAraclon Biotech S.L., Vía Hispanidad 21, 50009, Zaragoza, Spain.
Fernando GuillenServicio de Medicina Nuclear, Clínica Universidad de Navarra, Pamplona, Spain.
Inmaculada MonleónAraclon Biotech S.L., Vía Hispanidad 21, 50009, Zaragoza, Spain.
Itziar San-JoséAraclon Biotech S.L., Vía Hispanidad 21, 50009, Zaragoza, Spain.
Pablo Martínez-LageCenter for Research and Advanced Therapies and Memory Clinic, Fundación CITA-Alzheimer, San Sebastián, Spain.
Josep MunueraInstitut de recerca Sant Joan de Déu, Hospital Infantil Sant Joan de Déu, Barcelona, Spain.
Isabel HernándezResearch Center and Memory Clinic, Fundació ACE, Institut Català de Neurociències Aplicades, Universitat Internacional de Catalunya-Barcelona, Barcelona, Spain.
Mar BuendíaResearch Center and Memory Clinic, Fundació ACE, Institut Català de Neurociències Aplicades, Universitat Internacional de Catalunya-Barcelona, Barcelona, Spain.
Oscar Sotolongo-GrauResearch Center and Memory Clinic, Fundació ACE, Institut Català de Neurociències Aplicades, Universitat Internacional de Catalunya-Barcelona, Barcelona, Spain.
Montserrat AlegretResearch Center and Memory Clinic, Fundació ACE, Institut Català de Neurociències Aplicades, Universitat Internacional de Catalunya-Barcelona, Barcelona, Spain.
Agustín RuizResearch Center and Memory Clinic, Fundació ACE, Institut Català de Neurociències Aplicades, Universitat Internacional de Catalunya-Barcelona, Barcelona, Spain.
Lluis TárragaResearch Center and Memory Clinic, Fundació ACE, Institut Català de Neurociències Aplicades, Universitat Internacional de Catalunya-Barcelona, Barcelona, Spain.
Mercè BoadaResearch Center and Memory Clinic, Fundació ACE, Institut Català de Neurociències Aplicades, Universitat Internacional de Catalunya-Barcelona, Barcelona, Spain.
Manuel SarasaAraclon Biotech S.L., Vía Hispanidad 21, 50009, Zaragoza, Spain.
AB255 Study Group
SOM Biotech (Spain) · ESInstituto de Salud Carlos III · ESFundació ACE · ESHospital Sant Joan de Déu Barcelona · ES

Funding

Departament de Salut de la Generalitat RECERCALIA grant 390/06/2009Instituto de Salud Carlos III FISS PI10/00954
6 · The paper itself

Abstract

backgroundTo facilitate population screening and clinical trials of disease-modifying therapies for Alzheimer's disease, supportive biomarker information is necessary. This study was aimed to investigate the association of plasma amyloid-beta (Aβ) levels with the presence of pathological accumulation of Aβ in the brain measured by amyloid-PET. Both plasma Aβ42/40 ratio alone or combined with an FDG-PET-based biomarker of neurodegeneration were assessed as potential AD biomarkers.

methodsWe included 39 cognitively normal subjects and 20 patients with mild cognitive impairment from the AB255 Study who had undergone PiB-PET scans. Total Aβ40 and Aβ42 levels in plasma (TP42/40) were quantified using ABtest kits. Subjects were dichotomized as Aβ-PET positive or negative, and the ability of TP42/40 to detect Aβ-PET positivity was assessed by logistic regression and receiver operating characteristic analyses. Combination of plasma Aβ biomarkers and FDG-PET was further assessed as an improvement for brain amyloidosis detection and diagnosis classification.

resultsEighteen (30.5%) subjects were Aβ-PET positive. TP42/40 ratio alone identified Aβ-PET status with an area under the curve (AUC) of 0.881 (95% confidence interval [CI] = 0.779-0.982). Discriminating performance of TP42/40 to detect Aβ-PET-positive subjects yielded sensitivity and specificity values at Youden's cutoff of 77.8% and 87.5%, respectively, with a positive predictive value of 0.732 and negative predictive value of 0.900. All these parameters improved after adjusting the model for significant covariates. Applying TP42/40 as the first screening tool in a sequential diagnostic work-up would reduce the number of Aβ-PET scans by 64%. Combination of both FDG-PET scores and plasma Aβ biomarkers was found to be the most accurate Aβ-PET predictor, with an AUC of 0.965 (95% CI = 0.913-0.100).

conclusionsPlasma TP42/40 ratio showed a relevant and significant potential as a screening tool to identify brain Aβ positivity in preclinical and prodromal stages of Alzheimer's disease.

Indexed as

AgedAged, 80 and overAlzheimer DiseaseAmyloidAmyloid beta-PeptidesCognitive DysfunctionCross-Sectional StudiesFemaleFluorodeoxyglucose F18HumansLongitudinal StudiesMalePeptide FragmentsPositron-Emission TomographyAmyloidAmyloid beta-PeptidesFluorodeoxyglucose F18Peptide FragmentsAmyloid-betaAmyloid-PETBiomarkerFDG-PETMild cognitive impairmentPlasmaPreclinical Alzheimer’s disease

Identifiers

PMID31787105
PMCPMC6886187
OpenAlexW2990200033

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LicenceCC BY
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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.