Evidence map›Paper›PMID 39912369›Full record

ArticleSynapse (New York, N.Y.)2025

Synaptosomal-Associated Protein 25 kDA (SNAP-25) Levels in Cerebrospinal Fluid: Implications for Alzheimer's Disease Diagnosis and Monitoring.

Sofia Hjorth Wolner, Helena Sophia Gleerup, Christian Sandøe Musaeus, Peter Høgh, Nicholas J Ashton, Ann Brinkmalm, Johanna Nilsson, Lana Grötschel, Henrik Zetterberg, Kaj Blennow and 3 more

Abstract readEvaluation Study
PubMed Full text at PMC Publisher
In one paragraph

Article in Synapse (New York, N.Y.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Article
  2. Observational
  3. Review
  4. Review
  5. 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

13 authors.

Sofia Hjorth WolnerDanish Dementia Research Centre, Department of Neurology, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark.
Helena Sophia GleerupDanish Dementia Research Centre, Department of Neurology, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark.
Christian Sandøe MusaeusDanish Dementia Research Centre, Department of Neurology, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark.
Peter HøghRegional Dementia Research Centre, Department of Neurology, Zealand University Hospital, Roskilde, Denmark.
Nicholas J AshtonDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Ann BrinkmalmDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Johanna NilssonDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Lana GrötschelDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Henrik ZetterbergDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Kaj BlennowDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Steen Gregers HasselbalchDanish Dementia Research Centre, Department of Neurology, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark.
Anne Byriel WallsDepartment of Drug Design and Pharmacology, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
Anja Hviid SimonsenDanish Dementia Research Centre, Department of Neurology, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark.ORCID 0000-0002-5461-162X

Funding

Research Education ComponentP30AG072980 · NIA · BANNER HEALTH · PI Nicholas Ashton · 2021 to 2026
$24.9M
Absalon FoundationAD Strategic FundAlzheimer's Drug Discovery FoundationBluefield ProjectCure Alzheimer's FundEuropean Union Joint Programme - Neurodegenerative Disease ResearchEuropean Union's Horizon 2020 research and innovation programmeEuropean Union's Horizon EuropeFamiljen Erling-Perssons StiftelseFamiljen Rönströms StiftelseFondation pour la Recherche sur AlzheimerHjärnfondenKirsten and Freddy Johansen FoundationNational Institute for Health and Care Research University College London Hospitals Biomedical Research CentreNIA NIH HHS P30 AG072980Olav Thon StiftelsenStiftelsen för Gamla TjänarinnorSwedish Alzheimer FoundationSwedish Research CouncilUK Dementia Research Institute
6 · The paper itself

Abstract

Synaptic degeneration has been linked to cognitive decline. The presynaptic protein, synaptosomal-associated protein 25 kDA (SNAP-25), is crucial for synaptic transmission and has been suggested as a biomarker in Alzheimer's disease (AD). In the current study, we investigated the ability of SNAP-25 to differentiate between heterogenous dementia etiologies and whether SNAP-25 could be a staging marker in AD. SNAP-25 in the cerebrospinal fluid (CSF) from a retrospective (n = 187) and a prospective (n = 134) cohort was investigated with immunoprecipitation mass spectrometry (IP-MS) and single-molecule array (Simoa), respectively. Both cohorts consisted of healthy controls (HC) and patients with cognitive decline of different etiologies. CSF SNAP-25 concentration was higher in AD and non-neurodegenerative diseases (i.e., vascular dementia) compared with controls but did not differ between AD and non-AD neurodegenerative diseases. We found a trend toward an association between SNAP-25 and disease burden when comparing HC, mild cognitive impairment due to AD, and AD. CSF SNAP-25 concentrations were strongly associated with CSF phosphorylated tau (p-tau) concentrations, thus strengthening the link between synaptic dysfunction and tau pathophysiology in AD. Our initial findings suggest that SNAP-25 may be a potential biomarker for differentiating AD from dementia due to other etiologies. However, due to the significant association between SNAP-25 and p-tau proteins, the clinical utility of SNAP-25 as a diagnostic biomarker for AD may be limited, while SNAP-25 may be useful for monitoring disease progression or treatment response.

Indexed as

Alzheimer DiseaseDementiaSynaptosomal-Associated Protein 25AgedBiomarkersCross-Sectional StudiesDiagnosis, DifferentialDisease ProgressionFemaleHumansMaleMiddle AgedProspective StudiesRetrospective Studiestau ProteinsBiomarkersSNAP25 protein, humanSynaptosomal-Associated Protein 25tau ProteinsAlzheimer's diseaseCSFdiagnosisSNAP‐25

Identifiers

PMID39912369
PMCPMC11800177

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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.