Evidence map›Paper›PMID 39317877›Full record

ArticleJournal of neurology2024

Contactin proteins in cerebrospinal fluid show different alterations in dementias.

Besnik Muqaku, Sarah Anderl-Straub, Leonie Werner, Magdalena Nagl, Markus Otto, Charlotte E Teunissen, Patrick Oeckl

Abstract read
In one paragraph

Article in Journal of neurology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

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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

3 citing papers in PubMed.

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4 · The record

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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

7 authors.

Besnik MuqakuGerman Center for Neurodegenerative Diseases (DZNE E.V.), Helmholtzstr. 8/1, 89081, Ulm, Germany.
Sarah Anderl-StraubDepartment of Neurology, Ulm University Hospital, Helmholtzstr. 8/1, 89081, Ulm, Germany.
Leonie WernerDepartment of Neurology, Ulm University Hospital, Helmholtzstr. 8/1, 89081, Ulm, Germany.
Magdalena NaglDepartment of Neurology, Ulm University Hospital, Helmholtzstr. 8/1, 89081, Ulm, Germany.
Markus OttoDepartment of Neurology, Martin-Luther-University Halle-Wittenberg, Halle (Saale), Germany.
Charlotte E TeunissenNeurochemistry Laboratory, Department of Clinical Chemistry, Amsterdam University Medical Centers (UMC), Amsterdam, The Netherlands.
Patrick OecklGerman Center for Neurodegenerative Diseases (DZNE E.V.), Helmholtzstr. 8/1, 89081, Ulm, Germany. patrick.oeckl@uni-ulm.de.ORCID http://orcid.org/0000-0002-7652-7023

Funding

Alzheimer Forschung Initiative 20059CB
6 · The paper itself

Abstract

backgroundThe proteins contactin (CNTN) 1-6 are synaptic proteins for which there is evidence that they are dysregulated in neurodegenerative dementias. Less is known about CNTN changes and differences in cerebrospinal fluid (CSF) of dementias, which can provide important information about alterations of the CNTN network and be of value for differential diagnosis.

methodsWe developed a mass spectrometry-based multiple reaction monitoring (MRM) method to simultaneously determine all six CNTNs in CSF samples using stable isotope-labeled standard peptides. The analytical performance of the method was evaluated for peptide stability, dilution linearity and precision. CNTNs were measured in 82 CSF samples from patients with Alzheimer's disease (AD, n = 19), behavioural variant frontotemporal dementia (bvFTD, n = 18), Parkinson's disease dementia/dementia with Lewy bodies (PDD/DLB, n = 18) and non-neurodegenerative controls (n = 27) and compared with core AD biomarkers.

resultsThe MRM analysis revealed down-regulation of CNTN2 (fold change (FC) = 0.77), CNTN4 (FC = 0.75) and CNTN5 (FC = 0.67) in bvFTD and CNTN3 (FC = 0.72), CNTN4 (FC = 0.75) and CNTN5 (FC = 0.73) in PDD/DLB compared to AD. CNTN levels strongly correlated with each other in controls (r = 0.73), bvFTD (r = 0.86) and PDD/DLB (r = 0.70), but the correlation was significantly lower in AD (r = 0.41). CNTNs in AD did not show correlation even with core AD biomarkers. Combined use of CNTN1-6 levels increased diagnostic performance of AD core biomarkers.

conclusionsOur data show CNTNs differentially altered in dementias and indicate CNTN homeostasis being selectively dysregulated in AD. The combined use of CNTNs with AD core biomarkers might help to improve differential diagnosis.

Indexed as

BiomarkersContactinsDementiaAgedAged, 80 and overAlzheimer DiseaseFemaleFrontotemporal DementiaHumansLewy Body DiseaseMaleMass SpectrometryMiddle AgedParkinson DiseaseBiomarkersContactinsAlzheimer’s diseaseBiomarkerCerebrospinal fluidContactinDementiaSynaptic dysfunction

Identifiers

PMID39317877
PMCPMC11588959

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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.