Evidence map›Paper›PMID 31511058›Full record

ArticleAlzheimer's research & therapy2019

Discordant amyloid-β PET and CSF biomarkers and its clinical consequences.

Arno de Wilde, Juhan Reimand, Charlotte E Teunissen, Marissa Zwan, Albert D Windhorst, Ronald Boellaard, Wiesje M van der Flier, Philip Scheltens, Bart N M van Berckel, Femke Bouwman and 1 more

Abstract read
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 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

41 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Quantitative amyloid PET in Alzheimer's disease: the AMYPAD prognostic and natural history study.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2020
    Trial
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Considerations in the clinical use of amyloid PET and CSF biomarkers for Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Review
  10. New Research on Biomarkers in Alzheimer's Continuum.Reviews on recent clinical trials · 2025
    Review
  11. Article
  12. Article
  13. Article
  14. Observational
  15. Article
  16. Article
  17. Article
  18. Article
  19. Cerebral amyloid load determination in a clinical setting: interpretation of amyloid biomarker discordances aided by tau and neurodegeneration measurements.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2022
    Article
  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

11 authors.

Arno de WildeDepartment of Neurology & Alzheimer Center, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC, P.O. Box 7057, 1007 MB, Amsterdam, The Netherlands. arnodewilde@gmail.com.ORCID 0000-0002-3510-5510
Juhan ReimandDepartment of Neurology & Alzheimer Center, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC, P.O. Box 7057, 1007 MB, Amsterdam, The Netherlands.
Charlotte E TeunissenNeurochemistry laboratory, Department of Clinical Chemistry, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC, Amsterdam, The Netherlands.
Marissa ZwanDepartment of Neurology & Alzheimer Center, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC, P.O. Box 7057, 1007 MB, Amsterdam, The Netherlands.
Albert D WindhorstDepartment of Radiology & Nuclear Medicine, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC, Amsterdam, The Netherlands.
Ronald BoellaardDepartment of Radiology & Nuclear Medicine, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC, Amsterdam, The Netherlands.
Wiesje M van der FlierDepartment of Neurology & Alzheimer Center, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC, P.O. Box 7057, 1007 MB, Amsterdam, The Netherlands.
Philip ScheltensDepartment of Neurology & Alzheimer Center, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC, P.O. Box 7057, 1007 MB, Amsterdam, The Netherlands.
Bart N M van BerckelDepartment of Radiology & Nuclear Medicine, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC, Amsterdam, The Netherlands.
Femke BouwmanDepartment of Neurology & Alzheimer Center, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC, P.O. Box 7057, 1007 MB, Amsterdam, The Netherlands.
Rik OssenkoppeleDepartment of Neurology & Alzheimer Center, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC, P.O. Box 7057, 1007 MB, Amsterdam, The Netherlands.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIn vivo, high cerebral amyloid-β load has been associated with (i) reduced concentrations of Aβ

methodsWe included 768 patients (194 with subjective cognitive decline (SCD), 127 mild cognitive impairment (MCI), 309 Alzheimer's dementia (AD), and 138 non-AD) who were categorized as concordant-negative (n = 315, 41%), discordant (n = 97, 13%), or concordant-positive (n = 356, 46%) based on CSF and PET results. We compared discordant with both concordant-negative and concordant-positive groups on demographics, clinical syndrome, apolipoprotein E (APOE) ε4 status, CSF tau, and clinical and neuropsychological progression.

resultsWe found an increase from concordant-negative to discordant to concordant-positive in rates of APOE ε4 (28%, 55%, 70%, Z = - 10.6, P < 0.001), CSF total tau (25%, 45%, 78%, Z = - 13.7, P < 0.001), and phosphorylated tau (28%, 43%, 80%, Z = - 13.7, P < 0.001) positivity. In patients without dementia, linear mixed models showed that Mini-Mental State Examination and memory composite scores did not differ between concordant-negative (β [SE] - 0.13[0.08], P = 0.09) and discordant (β 0.08[0.15], P = 0.15) patients (P

conclusionsDiscordant cases were intermediate to concordant-negative and concordant-positive patients in terms of genetic (APOE ε4) and CSF (tau) markers of AD. While biomarker agreement did not impact cognition in patients with dementia, discordant biomarkers are not benign in patients without dementia given their higher risk of clinical progression.

Indexed as

Positron-Emission TomographyAgedAlzheimer DiseaseAmyloid beta-PeptidesApolipoprotein E4BiomarkersCognitive DysfunctionDiagnostic Self EvaluationFemaleHumansLongitudinal StudiesMaleMiddle AgedPeptide Fragmentstau ProteinsAmyloid beta-Peptidesamyloid beta-protein (1-42)Apolipoprotein E4BiomarkersPeptide Fragmentstau ProteinsAlzheimer’s diseaseAmyloidCerebrospinal fluidDementiaMild cognitive impairmentPositron emission tomographySubjective cognitive decline

Identifiers

PMID31511058
PMCPMC6739952

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.