Evidence map›Paper›PMID 34990894›Full record

ArticleEBioMedicine2022

Quantification of the trans-synaptic partners neurexin-neuroligin in CSF of neurodegenerative diseases by parallel reaction monitoring mass spectrometry.

Elena Camporesi, Johanna Nilsson, Agathe Vrillon, Emmanuel Cognat, Claire Hourregue, Henrik Zetterberg, Kaj Blennow, Bruno Becker, Ann Brinkmalm, Claire Paquet and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in EBioMedicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

11 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
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  5. Differences in blood levels of neuroligin-derived peptides in a cohort for early detection of Alzheimer's disease.The journals of gerontology. Series A, Biological sciences and medical sciences · 2026
    Article
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  7. Review
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  11. Role of Neurexins in Alzheimer's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    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 at 3 institutions in 3 countries.

Elena CamporesiInstitute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, the Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden; Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden. Electronic address: elena.camporesi@gu.se.
Johanna NilssonInstitute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, the Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden; Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden.
Agathe VrillonUniversité de Paris, Cognitive Neurology Center, GHU Nord APHP Hospital Lariboisière Fernand Widal, Paris, France; Université de Paris, Inserm UMR S11-44 Therapeutic Optimization in Neuropsychopharmacology, Paris, France.
Emmanuel CognatUniversité de Paris, Cognitive Neurology Center, GHU Nord APHP Hospital Lariboisière Fernand Widal, Paris, France; Université de Paris, Inserm UMR S11-44 Therapeutic Optimization in Neuropsychopharmacology, Paris, France.
Claire HourregueUniversité de Paris, Cognitive Neurology Center, GHU Nord APHP Hospital Lariboisière Fernand Widal, Paris, France.
Henrik ZetterbergInstitute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, the Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden; Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden; UK Dementia Research Institute at UCL, London, UK; Department of Neurodegenerative Disease, UCL Institute of Neurology, Queen Square, London, UK; Hong Kong Center for Neurodegenerative Diseases, Hong Kong, China.
Kaj BlennowInstitute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, the Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden; Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden.
Bruno BeckerInstitute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, the Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden; Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden.
Ann BrinkmalmInstitute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, the Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden; Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden.
Claire PaquetUniversité de Paris, Cognitive Neurology Center, GHU Nord APHP Hospital Lariboisière Fernand Widal, Paris, France; Université de Paris, Inserm UMR S11-44 Therapeutic Optimization in Neuropsychopharmacology, Paris, France.
Gunnar BrinkmalmInstitute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, the Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden; Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden.
Sahlgrenska University Hospital · SEInserm · FRUniversité Paris Cité · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSynaptic proteins are increasingly studied as biomarkers for synaptic dysfunction and loss, which are early and central events in Alzheimer's disease (AD) and strongly correlate with the degree of cognitive decline. In this study, we specifically investigated the synaptic binding partners neurexin (NRXN) and neuroligin (Nlgn) proteins, to assess their biomarker's potential.

methodswe developed a parallel reaction monitoring mass spectrometric method for the simultaneous quantification of NRXNs and Nlgns in cerebrospinal fluid (CSF) of neurodegenerative diseases, focusing on AD. Specifically, NRXN-1α, NRXN-1β, NRXN-2α, NRXN-3α and Nlgn1, Nlgn2, Nlgn3 and Nlgn4 proteins were targeted.

findingsThe proteins were investigated in a clinical cohort including CSF from controls (n=22), mild cognitive impairment (MCI) due to AD (n=44), MCI due to other conditions (n=46), AD (n=77) and a group of non-AD dementia (n=28). No difference in levels of NRXNs and Nlgns was found between AD (both at dementia and MCI stages) or controls or the non-AD dementia group for any of the targeted proteins. NRXN and Nlgn proteins correlated strongly with each other, but only a weak correlation with the AD core biomarkers and the synaptic biomarkers neurogranin and growth-associated protein 43, was found, possibly reflecting different pathogenic processing at the synapse.

interpretationwe conclude that NRXN and Nlgn proteins do not represent suitable biomarkers for synaptic pathology in AD. The panel developed here could aid in future investigations of the potential involvement of NRXNs and Nlgns in synaptic dysfunction in other disorders of the central nervous system.

fundinga full list of funding can be found under the acknowledgments section.

Indexed as

Alzheimer DiseaseCalcium-Binding ProteinsCell Adhesion Molecules, NeuronalCognitive DysfunctionNeural Cell Adhesion MoleculesNeurodegenerative DiseasesAmyloid beta-PeptidesBiomarkersHumansMass Spectrometrytau ProteinsAmyloid beta-PeptidesBiomarkersCalcium-Binding ProteinsCell Adhesion Molecules, NeuronalNeural Cell Adhesion Moleculesneuroligin 1NRXN1 protein, humantau ProteinsAlzheimer's diseasebiomarkersmass spectrometryneurexinsneuroliginssynaptic proteins

Identifiers

PMID34990894
PMCPMC8743209
OpenAlexW4206211980

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.