Evidence map›Paper›PMID 26383836›Full record

ArticleAlzheimer's research & therapy2015

Cerebrospinal fluid VILIP-1 and YKL-40, candidate biomarkers to diagnose, predict and monitor Alzheimer's disease in a memory clinic cohort.

Maartje I Kester, Charlotte E Teunissen, Courtney Sutphen, Elizabeth M Herries, Jack H Ladenson, Chengjie Xiong, Philip Scheltens, Wiesje M van der Flier, John C Morris, David M Holtzman and 1 more

Open access · goldAbstract read
In one paragraph

Article in Alzheimer's research & therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 7 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed, 7 pooled it
7.2field-weighted citation impact, top 2% 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

88 citing papers in PubMed, 7 syntheses or guidelines pooled it, 141 citations in OpenAlex.

  1. Pooled it
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  7. Pooled it
  8. Relationships of CSF biomarkers to cortical atrophy in early-onset Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
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  19. PeripheralFrontiers in aging neuroscience · 2025
    Article
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28 more citing papers are in PubMed but not listed here.

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 at 2 institutions in 2 countries.

Maartje I KesterAlzheimer Center and Department of Neurology, VU University Medical Center, PO box 7057, 1007 MB, Amsterdam, The Netherlands. m.kester@vumc.nl.
Charlotte E TeunissenDepartment of Clinical Chemistry, VU University Medical Center, Amsterdam, The Netherlands. c.teunissen@vumc.nl.
Courtney SutphenThe Knight Alzheimer's Disease Research Center, Washington University School of Medicine, 660 South Euclid, Campus Box 8111, St Louis, 63110, MO, USA. sutphenc@neuro.wustl.edu.
Elizabeth M HerriesDepartment of Pathology and Immunology, Washington University School of Medicine, 660 South Euclid, Campus Box 8111, St Louis, 63110, MO, USA. e.herries@wustl.edu.
Jack H LadensonDepartment of Pathology and Immunology, Washington University School of Medicine, 660 South Euclid, Campus Box 8111, St Louis, 63110, MO, USA. ladenson@wustl.edu.
Chengjie XiongThe Knight Alzheimer's Disease Research Center, Washington University School of Medicine, 660 South Euclid, Campus Box 8111, St Louis, 63110, MO, USA. chengjie@wubios.wustl.edu.
Philip ScheltensAlzheimer Center and Department of Neurology, VU University Medical Center, PO box 7057, 1007 MB, Amsterdam, The Netherlands. p.scheltens@vumc.nl.
Wiesje M van der FlierAlzheimer Center and Department of Neurology, VU University Medical Center, PO box 7057, 1007 MB, Amsterdam, The Netherlands. wm.vdflier@vumc.nl.
John C MorrisThe Knight Alzheimer's Disease Research Center, Washington University School of Medicine, 660 South Euclid, Campus Box 8111, St Louis, 63110, MO, USA. morrisj@abraxas.wustl.edu.
David M HoltzmanThe Knight Alzheimer's Disease Research Center, Washington University School of Medicine, 660 South Euclid, Campus Box 8111, St Louis, 63110, MO, USA. holtzman@neuro.wustl.edu.
Anne M FaganThe Knight Alzheimer's Disease Research Center, Washington University School of Medicine, 660 South Euclid, Campus Box 8111, St Louis, 63110, MO, USA. fagana@neuro.wustl.edu.
Washington University in St. Louis · USAmsterdam UMC Location VUmc · NL

Funding

Smartphone-Based "Burst" Cognitive AssessmentsP01AG003991 · NIA · WASHINGTON UNIVERSITY · PI Tammie Lee Smith Benzinger · 1985 to 2026
$69.5M
Imaging CoreU19AG032438 · NIA · WASHINGTON UNIVERSITY · PI BATEMAN, RANDALL J · 2010 to 2025
$53.9M
WASHINGTON UNIVERSITY ALZHEIMERS DISEASE RESEARCH CENTERP50AG005681 · NIA · WASHINGTON UNIVERSITY · PI MORRIS, JOHN · 1985 to 2019
$52.1M
The natural history of AB accumulation in preclinical ADP01AG026276 · NIA · WASHINGTON UNIVERSITY · PI SCHINDLER, SUZANNE ELIZABETH · 2005 to 2025
$49.5M
NIA NIH HHS P01 AG003991NIA NIH HHS P01 AG026276NIA NIH HHS P50 AG005681NIA NIH HHS U19 AG032438
6 · The paper itself

Abstract

introductionWe examined the utility of cerebrospinal fluid (CSF) proteins, Chitinase-3-like protein 1 (CHI3L1 or YKL-40), a putative marker of inflammation, and Visinin-like protein-1 (VILIP-1), a marker for neuronal injury, for diagnostic classification and monitoring of disease progression in a memory clinic cohort.

methodsCSF levels of YKL-40 and VILIP-1 were measured in 37 cognitively normal, 61 Mild Cognitive Impairment (MCI) and 65 Alzheimer's disease (AD) patients from the memory clinic-based Amsterdam Dementia Cohort who underwent two lumbar punctures, with minimum interval of 6 months and a mean (SE) interval of 2.0(0.1) years. Mean(SE) cognitive follow-up was 3.8 (0.2) years. ANOVA was used to compare baseline differences of log-transformed CSF measures. Cox proportional hazard models were used to evaluate disease progression as a function of CSF tertiles. Linear mixed models were used to evaluate longitudinal change over time. All analyses were sex and age adjusted.

resultsBaseline levels of YKL-40, but not VILIP-1, were higher in MCI and AD patients compared to cognitively normal individuals (mean (SE) pg/mL, 304 (16) and 288 (12) vs. 231 (16), p = 0.03 and p = 0.006). Baseline levels of both YKL-40 and VILIP-1 in MCI predicted progression to AD (HR 95% CI = 3.0 (1.1-7.9) and 4.4 (1.5-13.0), respectively, for highest vs. lowest tertile). YKL-40 increased longitudinally in patients with MCI and AD (mean (SE) pg/mL per year, 8.9 (3.0) and 7.1 (3.1), respectively), but not in cognitively normal individuals, whereas levels of VILIP-1 increased only in MCI (mean (SE), 10.7 (2.6) pg/mL per year).

conclusionsCSF levels of YKL-40 may have utility for discriminating between cognitively normal individuals and patients with MCI or AD. Increased levels of both YKL-40 and VILIP-1 may be associated with disease progression. These CSF biomarkers should be considered for future evaluation in the characterization of the natural history of AD.

Indexed as

AdipokinesAgedAlzheimer DiseaseAnalysis of VarianceBiomarkersChitinase-3-Like Protein 1Cognitive DysfunctionCross-Sectional StudiesDisease ProgressionFemaleFollow-Up StudiesHumansKaplan-Meier EstimateLectinsLinear ModelsLongitudinal StudiesAdipokinesBiomarkersCHI3L1 protein, humanChitinase-3-Like Protein 1LectinsNeurocalcinVSNL1 protein, human

Identifiers

PMID26383836
PMCPMC4574487
OpenAlexW1931861387

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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.