Evidence map›Paper›PMID 25559750›Full record

ArticleNeuropathology and applied neurobiology2015

Synaptic protein levels altered in vascular dementia.

Lindsey I Sinclair, Hannah M Tayler, Seth Love

Open access · hybridAbstract read
In one paragraph

Article in Neuropathology and applied neurobiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 3 pooled it
5.7field-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

41 citing papers in PubMed, 3 syntheses or guidelines pooled it, 86 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. The enigma of vascular dementia: current state and emerging perspectives.Journal of neural transmission (Vienna, Austria : 1996) · 2026
    Review
  5. Exploring synaptic density patterns in cerebral small vessel disease: insights from [European journal of nuclear medicine and molecular imaging · 2026
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Hepatic Encephalopathy and Melatonin.Antioxidants (Basel, Switzerland) · 2022
    Review
  15. Review
  16. Frontiers in aging neuroscience · 2022
    Article
  17. Article
  18. Article
  19. Article
  20. Review
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

3 authors at 1 institution in 1 country.

Lindsey I SinclairSchool of Social and Community Medicine, University of Bristol, Bristol, UK.
Hannah M TaylerSchool of Clinical Sciences, University of Bristol, Bristol, UK.
Seth LoveSchool of Clinical Sciences, University of Bristol, Bristol, UK.
University of Bristol · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

introductionCerebral ischaemia is the defining pathophysiological abnormality in most forms of vascular dementia (VAD), but the pathogenesis of the dementia remains poorly understood. In Alzheimer's disease (AD), there is early loss of synaptic proteins, but these have been little studied in VAD. MATERIALS AND

methodsWe measured synaptophysin, postsynaptic density protein 95 (PSD-95), drebrin, synaptosomal-associated protein 25 (SNAP-25) and vascular endothelial growth factor (VEGF) by enzyme-linked immunosorbent assays in superior temporal cortex from 11 patients with VAD and, initially, 11 non-dementia controls. We corrected for neuronal content by measurement of neuron-specific enolase. A further 11 controls were subsequently used in a validation study. Simulation of post-mortem delay found that PSD-95 was stable at 4°C but declined slightly at RT. SNAP-25 and drebrin showed good post-mortem stability. Previous studies had shown good post-mortem preservation of synaptophysin and VEGF.

resultsThe VAD cases had lower synaptophysin (but P > 0.05 in initial study), significantly lower SNAP-25 (P = 0.024) and significantly higher drebrin (P = 0.020). On comparison with the second control group, the reduction in synaptophysin was significant (P = 0.008), and the other results were confirmed.

conclusionThere is probably a reduction in presynaptic proteins in the temporal cortex in VAD, although not as marked as in AD. In VAD, there is also an increase in drebrin, which may be a response to reduced synaptic input.

Indexed as

AgedAged, 80 and overDementia, VascularDisks Large Homolog 4 ProteinFemaleHumansIntracellular Signaling Peptides and ProteinsMaleMembrane ProteinsNeuropeptidesSynapsesSynaptophysinSynaptosomal-Associated Protein 25Temporal LobeVascular Endothelial Growth Factor ADisks Large Homolog 4 ProteinDLG4 protein, humandrebrinsIntracellular Signaling Peptides and ProteinsMembrane ProteinsNeuropeptidesSNAP25 protein, humanSynaptophysinSynaptosomal-Associated Protein 25SYP protein, humanVascular Endothelial Growth Factor Aapolipoproteins EDLG4 protein humandrebrinsSNAP 25 protein humansynaptophysinvascular dementia

Identifiers

PMID25559750
PMCPMC4471617
OpenAlexW1569894857

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.