Evidence map›Paper›PMID 27605218›Full record

ArticleMolecular neurodegeneration2016

No diurnal variation of classical and candidate biomarkers of Alzheimer's disease in CSF.

Claudia Cicognola, Davide Chiasserini, Paolo Eusebi, Ulf Andreasson, Hugo Vanderstichele, Henrik Zetterberg, Lucilla Parnetti, Kaj Blennow

Abstract read
In one paragraph

Article in Molecular neurodegeneration, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
–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

14 citing papers in PubMed.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Tau kinetics in Alzheimer's disease.Frontiers in aging neuroscience · 2022
    Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. The "glymphatic" mechanism for solute clearance in Alzheimer's disease: game changer or unproven speculation?FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018
    Review
  11. Review
  12. Article
  13. Article
  14. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors.

Claudia CicognolaInstitute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at University of Gothenburg, House V3, SU / Mölndal hospital, Göteborgsvägen 31, SE-431 80, Mölndal, Sweden.
Davide ChiasseriniSection of Neurology, Department of Medicine, Center for Memory Disturbances, University of Perugia, Sant' Andrea delle Fratte, 06132, Perugia, Italy.
Paolo EusebiSection of Neurology, Department of Medicine, Center for Memory Disturbances, University of Perugia, Sant' Andrea delle Fratte, 06132, Perugia, Italy.
Ulf AndreassonInstitute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at University of Gothenburg, House V3, SU / Mölndal hospital, Göteborgsvägen 31, SE-431 80, Mölndal, Sweden.
Hugo VandersticheleADx NeuroSciences, Gent, Belgium.
Henrik ZetterbergInstitute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at University of Gothenburg, House V3, SU / Mölndal hospital, Göteborgsvägen 31, SE-431 80, Mölndal, Sweden.
Lucilla ParnettiSection of Neurology, Department of Medicine, Center for Memory Disturbances, University of Perugia, Sant' Andrea delle Fratte, 06132, Perugia, Italy. lucilla.parnetti@unipg.it.
Kaj BlennowInstitute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at University of Gothenburg, House V3, SU / Mölndal hospital, Göteborgsvägen 31, SE-431 80, Mölndal, Sweden.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCerebrospinal fluid (CSF) biomarkers have gained increasing importance in the diagnostic work-up of Alzheimer's disease (AD). The core CSF biomarkers related to AD pathology (Aβ42, t-tau and p-tau) are currently used in CSF diagnostics, while candidate markers of amyloid metabolism (Aβ38, Aβ40, sAPPα, sAPPβ), synaptic loss (neurogranin), neuroinflammation (YKL-40), neuronal damage (VILIP-1) and genetic risk (apolipoprotein E) are undergoing evaluation. Diurnal fluctuation in the concentration of CSF biomarkers has been reported and may represent a preanalytical confounding factor in the laboratory diagnosis of AD. The aim of the present study was to investigate the diurnal variability of classical and candidate CSF biomarkers in a cohort of neurosurgical patients carrying a CSF drainage.

methodSamples were collected from a cohort of 13 neurosurgical patients from either ventricular (n = 6) or lumbar (n = 7) CSF drainage at six time points during the day, 1-7 days following the neurosurgical intervention. Concentrations of the core biomarkers were determined by immunoassays.

resultsAlthough absolute values largely varied among subjects, none of the biomarkers showed significant diurnal variation. Site of drainage (lumbar vs. ventricular) did not influence this result. The different immunoassays used for tau and Aβ markers provided similar results.

conclusionTime of day at CSF collection does not ultimately affect the concentration levels of classical and candidate AD biomarkers. Similar trends were found when using different immunoassays, thus corroborating the consistency of the data.

Indexed as

AdultAgedAlzheimer DiseaseAmyloid beta-PeptidesApolipoproteins EBiomarkersFemaleHumansMaleMiddle AgedPeptide Fragmentstau ProteinsAmyloid beta-PeptidesApolipoproteins EBiomarkersPeptide Fragmentstau Proteins

Identifiers

PMID27605218
PMCPMC5013624

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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.