Evidence map›Paper›PMID 38970402›Full record

ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2024

CSF proteomic profiles of neurodegeneration biomarkers in Alzheimer's disease.

Aurore Delvenne, Johan Gobom, Suzanne E Schindler, Mara Ten Kate, Lianne M Reus, Valerija Dobricic, Betty M Tijms, Tammie L S Benzinger, Carlos Cruchaga, Charlotte E Teunissen and 19 more

Abstract read
In one paragraph

Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. CSF proteomic profiles of neurodegeneration biomarkers in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    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

29 authors.

Aurore DelvenneDepartment of Psychiatry and Neuropsychology, Alzheimer Centrum Limburg, School for Mental Health and Neuroscience, Maastricht University, Maastricht, the Netherlands.ORCID 0000-0001-8724-3010
Johan GobomClinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden.
Suzanne E SchindlerDepartment of Neurology, Washington University School of Medicine, St. Louis, Missouri, USA.
Mara Ten KateAlzheimer Center Amsterdam, Department of Neurology, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC, Amsterdam, the Netherlands.
Lianne M ReusAlzheimer Center Amsterdam, Department of Neurology, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC, Amsterdam, the Netherlands.
Valerija DobricicLübeck Interdisciplinary Platform for Genome Analytics, University of Lübeck, Lübeck, Germany.
Betty M TijmsAlzheimer Center Amsterdam, Department of Neurology, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC, Amsterdam, the Netherlands.
Tammie L S BenzingerDepartment of Radiology, Washington University School of Medicine, St. Louis, Missouri, USA.
Carlos CruchagaDepartment of Psychiatry, Washington University School of Medicine, St. Louis, Missouri, USA.
Charlotte E TeunissenNeurochemistry Laboratory, Department of Clinical Chemistry, Amsterdam University Medical Centers (AUMC), Amsterdam Neuroscience, Amsterdam, the Netherlands.
Inez RamakersDepartment of Psychiatry and Neuropsychology, Alzheimer Centrum Limburg, School for Mental Health and Neuroscience, Maastricht University, Maastricht, the Netherlands.
Pablo Martinez-LageFundación CITA-Alzhéimer Fundazioa, Donostia, Spain.
Mikel TaintaFundación CITA-Alzhéimer Fundazioa, Donostia, Spain.
Rik VandenbergheNeurology Service, University Hospitals Leuven, Leuven, Belgium.
Jolien SchaeverbekeNeurology Service, University Hospitals Leuven, Leuven, Belgium.
Sebastiaan EngelborghsReference Center for Biological Markers of Dementia (BIODEM), Department of Biomedical Sciences, University of Antwerp, Antwerp, Belgium.
Ellen De RoeckReference Center for Biological Markers of Dementia (BIODEM), Department of Biomedical Sciences, University of Antwerp, Antwerp, Belgium.
Julius PoppOld Age Psychiatry, University Hospital Lausanne, Lausanne, Switzerland.
Gwendoline PeyratoutOld Age Psychiatry, University Hospital Lausanne, Lausanne, Switzerland.
Magda Tsolaki1st Department of Neurology, AHEPA University Hospital, Medical School, Faculty of Health Sciences, Aristotle University of Thessaloniki, Makedonia, Thessaloniki, Greece.
Yvonne Freund-LeviDepartment of Neurobiology, Caring Sciences and Society (NVS), Division of Clinical Geriatrics, Karolinska Institutet, Huddinge, Stockholm, Sweden.
Simon LovestoneUniversity of Oxford, United Kingdom (currently at Johnson and Johnson Medical Ltd., Oxford, UK.
Johannes StrefferReference Center for Biological Markers of Dementia (BIODEM), Department of Biomedical Sciences, University of Antwerp, Antwerp, Belgium.
Frederik BarkhofAlzheimer Center Amsterdam, Department of Neurology, Amsterdam Neuroscience, Vrije Universiteit Amsterdam, Amsterdam UMC, Amsterdam, the Netherlands.
Lars BertramLübeck Interdisciplinary Platform for Genome Analytics, University of Lübeck, Lübeck, Germany.
Kaj BlennowClinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden.
Henrik ZetterbergClinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden.
Pieter Jelle VisserDepartment of Psychiatry and Neuropsychology, Alzheimer Centrum Limburg, School for Mental Health and Neuroscience, Maastricht University, Maastricht, the Netherlands.
Stephanie J B VosDepartment of Psychiatry and Neuropsychology, Alzheimer Centrum Limburg, School for Mental Health and Neuroscience, Maastricht University, Maastricht, the Netherlands.

Funding

Smartphone-Based "Burst" Cognitive AssessmentsP01AG003991 · NIA · WASHINGTON UNIVERSITY · PI CHENGJIE XIONG · 1985 to 2026
$69.5M
The natural history of AB accumulation in preclinical ADP01AG026276 · NIA · WASHINGTON UNIVERSITY · PI MORRIS, JOHN · 2005 to 2025
$49.5M
Research Education ComponentP30AG066444 · NIA · WASHINGTON UNIVERSITY · PI DAVID M. HOLTZMAN · 2020 to 2026
$28.7M
STAGING PRECLINICAL AD WITH CSF BIOMARKERSK23AG053426 · NIA · WASHINGTON UNIVERSITY · PI SCHINDLER, SUZANNE ELIZABETH · 2017 to 2020
$654k
anonymous foundationEMIF-AD MBDNIA NIH HHS K23 AG053426NIA NIH HHS P01 AG003991NIA NIH HHS P01 AG026276NIA NIH HHS P30 AG066444ZonMw (Memorabel program) 733050502ZonMw (Memorabel program) 7330505021
6 · The paper itself

Abstract

introductionWe aimed to unravel the underlying pathophysiology of the neurodegeneration (N) markers neurogranin (Ng), neurofilament light (NfL), and hippocampal volume (HCV), in Alzheimer's disease (AD) using cerebrospinal fluid (CSF) proteomics.

methodsIndividuals without dementia were classified as A+ (CSF amyloid beta [Aβ]42), T+ (CSF phosphorylated tau181), and N+ or N- based on Ng, NfL, or HCV separately. CSF proteomics were generated and compared between groups using analysis of covariance.

resultsOnly a few individuals were A+T+Ng-. A+T+Ng+ and A+T+NfL+ showed different proteomic profiles compared to A+T+Ng- and A+T+NfL-, respectively. Both Ng+ and NfL+ were associated with neuroplasticity, though in opposite directions. Compared to A+T+HCV-, A+T+HCV+ showed few proteomic changes, associated with oxidative stress. DISCUSSION: Different N markers are associated with distinct neurodegenerative processes and should not be equated. N markers may differentially complement disease staging beyond amyloid and tau. Our findings suggest that Ng may not be an optimal N marker, given its low incongruency with tau pathophysiology. HIGHLIGHTS: In Alzheimer's disease, neurogranin (Ng)+, neurofilament light (NfL)+, and hippocampal volume (HCV)+ showed differential protein expression in cerebrospinal fluid. Ng+ and NfL+ were associated with neuroplasticity, although in opposite directions. HCV+ showed few proteomic changes, related to oxidative stress. Neurodegeneration (N) markers may differentially refine disease staging beyond amyloid and tau. Ng might not be an optimal N marker, as it relates more closely to tau.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesBiomarkersHippocampusNeurofilament ProteinsNeurograninProteomicstau ProteinsAgedFemaleHumansMaleMiddle AgedPeptide FragmentsAmyloid beta-Peptidesamyloid beta-protein (1-42)Biomarkersneurofilament protein LNeurofilament ProteinsNeurograninPeptide Fragmentstau ProteinsAlzheimer's diseasebiomarkerscerebrospinal fluidhippocampal volumeneurodegeneration markersneurofilament lightneurograninpathophysiologyproteomics

Identifiers

PMID38970402
PMCPMC11497678

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

None linked

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.