Evidence map›Paper›PMID 29378650›Full record

ArticleAlzheimer's research & therapy2018

Assessment of kallikrein 6 as a cross-sectional and longitudinal biomarker for Alzheimer's disease.

Kalicharan Patra, Antoninus Soosaipillai, Sigrid Botne Sando, Camilla Lauridsen, Guro Berge, Ina Møller, Gøril Rolfseng Grøntvedt, Geir Bråthen, Ilijana Begcevic, Simon Moussaud and 5 more

Open access · goldAbstract read
In one paragraph

Article in Alzheimer's research & therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

28 citing papers in PubMed, 39 citations in OpenAlex.

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  6. Drug Discovery Strategies for Kallikrein-Related Peptidases.International journal of molecular sciences · 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

15 authors at 6 institutions in 3 countries.

Kalicharan PatraDepartment of Neurochemistry, Stockholm University, Svante Arrhenius väg 16B, 106 91, Stockholm, Sweden.
Antoninus SoosaipillaiDepartment of Pathology and Laboratory Medicine, Lunenfeld-Tanenbaum Research Institute-Mount Sinai Hospital, Toronto, ON, Canada.
Sigrid Botne SandoDepartment of Neurology, University Hospital of Trondheim, Trondheim, Norway.
Camilla LauridsenDepartment of Neuromedicine and Movement Science, Norwegian University of Science and Technology, Trondheim, Norway.
Guro BergeDepartment of Neuromedicine and Movement Science, Norwegian University of Science and Technology, Trondheim, Norway.
Ina MøllerDepartment of Neuromedicine and Movement Science, Norwegian University of Science and Technology, Trondheim, Norway.
Gøril Rolfseng GrøntvedtDepartment of Neuromedicine and Movement Science, Norwegian University of Science and Technology, Trondheim, Norway.
Geir BråthenDepartment of Neurology, University Hospital of Trondheim, Trondheim, Norway.
Ilijana BegcevicDepartment of Pathology and Laboratory Medicine, Lunenfeld-Tanenbaum Research Institute-Mount Sinai Hospital, Toronto, ON, Canada.
Simon MoussaudDepartment of Neurochemistry, Stockholm University, Svante Arrhenius väg 16B, 106 91, Stockholm, Sweden.
Lennart MinthonDepartment of Clinical Sciences, Lund University, Lund, Sweden.
Oskar HanssonDepartment of Clinical Sciences, Lund University, Lund, Sweden.
Eleftherios P DiamandisDepartment of Pathology and Laboratory Medicine, Lunenfeld-Tanenbaum Research Institute-Mount Sinai Hospital, Toronto, ON, Canada.
Linda R WhiteDepartment of Neurology, University Hospital of Trondheim, Trondheim, Norway.
Henrietta M NielsenDepartment of Neurochemistry, Stockholm University, Svante Arrhenius väg 16B, 106 91, Stockholm, Sweden. henrietta.nielsen@neurochem.su.se.
Norwegian University of Science and Technology · NOStockholm University · SELund University · SELunenfeld-Tanenbaum Research Institute · CAMount Sinai Hospital · CASt Olav's University Hospital · NO

Funding

Alzheimer's Association 2015-NIRG-339824VINNMER/ Marie Curie Fellowship 2015-04905
6 · The paper itself

Abstract

backgroundKallikrein 6 (KLK6) is known to be an age-related protease expressed at high levels in the central nervous system. It was previously shown to be involved in proteolysis of extracellular proteins implicated in neurodegenerative diseases such as Alzheimer's disease (AD), prompting validation of KLK6 as a potential biomarker of disease. However, analyses of both plasma and cerebrospinal fluid (CSF) levels of KLK6 in patients with AD have been inconclusive. We present a detailed analysis of KLK6 in plasma and CSF in two separate cohorts in a cross-sectional and a longitudinal clinical setting.

methodsThe cross-sectional cohort included control subjects without dementia and patients with AD, and the longitudinal cohort included patients with MCI and patients with AD followed over a 2-year period. Plasma and CSF levels of KLK6 were quantified by use of a previously developed and validated enzyme-linked immunosorbent assay. Statistical analyses were performed to compare KLK6 levels between diagnostic groups and to identify potential associations between KLK6 level, age, apolipoprotein E (APOE) genotype, total apoE level and the classical CSF AD biomarkers.

resultsIn the cross-sectional setting, KLK6 levels in plasma but not in CSF were significantly higher in the AD group than in control subjects. CSF but not plasma KLK6 levels were positively correlated with age in both the cross-sectional and longitudinal settings. In both cohorts, the CSF KLK6 levels were significantly and positively correlated with the CSF levels of core AD biomarkers. Total plasma and CSF apoE levels were positively associated with KLK6 in the cross-sectional study. Finally, during the 2-year monitoring period of the longitudinal cohort, CSF KLK6 levels increased with disease progression over time in the investigated patient groups.

conclusionsIn two separate cohorts we have confirmed the previously reported correlation between age and CSF levels of KLK6. Increased plasma KLK6 levels in patients with AD with a more advanced disease stage suggest KLK6 as a potential biomarker in patients with AD with more severe dementia. Significant correlations between KLK6 levels and core CSF AD biomarkers suggest molecular links between KLK6 and AD-related pathological processes.

Indexed as

AdultAgedAged, 80 and overAlzheimer DiseaseApolipoprotein E4BiomarkersCross-Sectional StudiesFemaleHumansKallikreinsLongitudinal StudiesMaleMental Status and Dementia TestsMiddle AgedApolipoprotein E4BiomarkersKallikreinsKLK6 protein, humanAlzheimer’s diseaseBiomarkerKLK6NeurodegenerationNeurosin

Identifiers

PMID29378650
PMCPMC5789599
OpenAlexW2790746318

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LicenceCC BY
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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.