Evidence map›Paper›PMID 31847891›Full record

ArticleAlzheimer's research & therapy2019

CSF synaptic protein concentrations are raised in those with atypical Alzheimer's disease but not frontotemporal dementia.

Mica T M Clarke, Ann Brinkmalm, Martha S Foiani, Ione O C Woollacott, Carolin Heller, Amanda Heslegrave, Ashvini Keshavan, Nick C Fox, Jonathan M Schott, Jason D Warren and 3 more

Open access · goldAbstract read
In one paragraph

Article in Alzheimer's research & therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
5.2field-weighted citation impact, top 4% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.

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  5. Development and validation of a novel Simoa assay for NPTX2 in Alzheimer's disease and Down syndrome.Alzheimer's & dementia : the journal of the Alzheimer's Association · 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

13 authors at 3 institutions in 2 countries.

Mica T M ClarkeDementia Research Centre, Department of Neurodegenerative Disease, University College London, Queen Square Institute of Neurology, London, WC1N 3BG, UK.
Ann BrinkmalmDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Martha S FoianiUK Dementia Research Institute at UCL, London, UK.
Ione O C WoollacottDementia Research Centre, Department of Neurodegenerative Disease, University College London, Queen Square Institute of Neurology, London, WC1N 3BG, UK.
Carolin HellerUK Dementia Research Institute at UCL, London, UK.
Amanda HeslegraveUK Dementia Research Institute at UCL, London, UK.
Ashvini KeshavanDementia Research Centre, Department of Neurodegenerative Disease, University College London, Queen Square Institute of Neurology, London, WC1N 3BG, UK.
Nick C FoxDementia Research Centre, Department of Neurodegenerative Disease, University College London, Queen Square Institute of Neurology, London, WC1N 3BG, UK.
Jonathan M SchottDementia Research Centre, Department of Neurodegenerative Disease, University College London, Queen Square Institute of Neurology, London, WC1N 3BG, UK.
Jason D WarrenDementia Research Centre, Department of Neurodegenerative Disease, University College London, Queen Square Institute of Neurology, London, WC1N 3BG, UK.
Kaj BlennowDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Henrik ZetterbergDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Jonathan D RohrerDementia Research Centre, Department of Neurodegenerative Disease, University College London, Queen Square Institute of Neurology, London, WC1N 3BG, UK. j.rohrer@ucl.ac.uk.ORCID 0000-0002-6155-8417
UK Dementia Research Institute · GBSahlgrenska University Hospital · SEUniversity of Gothenburg · SE

Funding

Medical Research Council MR/M008525/1Medical Research Council MR/M018288/1
6 · The paper itself

Abstract

backgroundIncreased CSF levels of a number of synaptic markers have been reported in Alzheimer's disease (AD), but little is known about their concentrations in frontotemporal dementia (FTD). We investigated this in three synaptic proteins, neurogranin, SNAP-25, and synaptotagmin-1.

methodsCSF samples were analysed from 66 patients with a disorder in the FTD spectrum and 19 healthy controls. Patients were stratified by their tau to Aβ

resultsThe AD biomarker group had significantly higher concentrations of all synaptic proteins compared to controls except for synaptotagmin-1 where there was only a trend to increased levels-Ng22, AD mean 232.2 (standard deviation 138.9) pg/ml, controls 137.6 (95.9); Ng36, 225.5 (148.8) pg/ml, 130.0 (80.9); SNAP-25tot, 71.4 (27.9) pM, 53.5 (11.7); SNAP-25aa40, 14.0 (6.3), 7.9 (2.3) pM; and synaptotagmin-1, 287.7 (156.0) pM, 238.3 (71.4). All synaptic measures were significantly higher in the atypical AD group than the FTD biomarker group except for Ng36 where there was only a trend to increased levels-Ng22, 114.0 (117.5); Ng36, 171.1 (75.2); SNAP-25tot, 49.2 (16.7); SNAP-25aa40, 8.2 (3.4); and synaptotagmin-1, 197.1 (78.9). No markers were higher in the FTD biomarker group than controls. No significant differences were seen in the subgroup analysis, but there was a trend to increased levels in those with likely tau pathology.

conclusionsNo CSF synaptic proteins have been shown to be abnormal in those with likely FTD pathologically. Higher CSF synaptic protein concentrations of neurogranin, SNAP-25, and synaptotagmin-1 appear to be related to AD pathology.

Indexed as

AgedAlzheimer DiseaseAmyloid beta-PeptidesBiomarkersFemaleFrontotemporal DementiaHumansMaleMiddle AgedNeurograninPeptide FragmentsSynaptosomal-Associated Protein 25Synaptotagmin Itau ProteinsAmyloid beta-Peptidesamyloid beta-protein (1-42)BiomarkersNeurograninPeptide FragmentsSynaptosomal-Associated Protein 25Synaptotagmin Itau ProteinsAlzheimer’s diseaseBiomarkersFrontotemporal dementiaNeurograninSNAP-25SynapticSynaptotagmin-1

Identifiers

PMID31847891
PMCPMC6918699
OpenAlexW2996155157

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.