Evidence map›Paper›PMID 30115118›Full record

ArticleAlzheimer's research & therapy2018

Cerebrospinal fluid synaptosomal-associated protein 25 is a key player in synaptic degeneration in mild cognitive impairment and Alzheimer's disease.

Hua Zhang, Joseph Therriault, Min Su Kang, Kok Pin Ng, Tharick A Pascoal, Pedro Rosa-Neto, Serge Gauthier, Alzheimer’s Disease Neuroimaging Initiative

Open access · goldAbstract read
In one paragraph

Article in Alzheimer's research & therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 2 pooled it
4.4field-weighted citation impact, top 5% 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

56 citing papers in PubMed, 2 syntheses or guidelines pooled it, 92 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Relationships of CSF biomarkers to cortical atrophy in early-onset Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. 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

8 authors at 3 institutions in 3 countries.

Hua ZhangDepartment of Neurology, the First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Joseph TherriaultThe McGill University Research Centre for Studies in Aging, McGill University, Montreal, Canada.
Min Su KangThe McGill University Research Centre for Studies in Aging, McGill University, Montreal, Canada.
Kok Pin NgDepartment of Neurology, National Neuroscience Institute, Singapore, Singapore.
Tharick A PascoalThe McGill University Research Centre for Studies in Aging, McGill University, Montreal, Canada.
Pedro Rosa-NetoThe McGill University Research Centre for Studies in Aging, McGill University, Montreal, Canada.
Serge GauthierThe McGill University Research Centre for Studies in Aging, McGill University, Montreal, Canada. serge.gauthier@mcgill.ca.
Alzheimer’s Disease Neuroimaging Initiative
McGill University · CANational Neuroscience Institute · SGThe Affiliated Yongchuan Hospital of Chongqing Medical University · CN

Funding

Alzheimer's Disease Neuroimaging Initiative - SupplementU01AG024904 · NIA · NORTHERN CALIFORNIA INSTITUTE RES &EDUC · PI WEINER, MICHAEL W · 2004 to 2015
$121.0M
Fonds de Recherche du Québec - Santé FRQS; Chercheur BoursierNIA NIH HHS U01 AG024904the Alzheimer's Association NIRG-12- 92090, NIRP-12-259245Weston Brain Institute, Canadian Institutes of Health Research (CIHR) MOP-11-51-31
6 · The paper itself

Abstract

backgroundThere is accumulating evidence that synaptic loss precedes neuronal loss and correlates best with impaired memory formation in Alzheimer's disease (AD). Cerebrospinal fluid (CSF) synaptosomal-associated protein 25 (SNAP-25) is a newly discovered marker indicating synaptic damage. We here test CSF SNAP-25 and SNAP-25/amyloid-β42 (Aβ42) ratio as a diagnostic marker for predicting cognitive decline and brain structural change in the Alzheimer's Disease Neuroimaging Initiative (ADNI) database.

methodsWe stratified 139 participants from the ADNI database into cognitively normal (CN; n = 52), stable mild cognitive impairment (sMCI; n = 22), progressive MCI (pMCI; n = 47), and dementia due to AD (n = 18). Spearman correlation was performed to test the relationships between biomarkers. Overall diagnostic accuracy (area under the curve (AUC)) was obtained from receiver operating curve (ROC) analyses. Cox proportional hazard models tested the effect of CSF SNAP-25 and SNAP-25/Aβ42 measures on the conversion from MCI to AD. Relationships between the CSF SNAP-25 levels, SNAP-25/Aβ42 ratio, and diagnostic groups were tested with linear regressions. Linear mixed-effects models and linear regression models were used to evaluate CSF SNAP-25 and SNAP-25/Aβ42 as predictors of AD features, including cognition measured by the Mini-Mental State Examination (MMSE) and brain structure and white matter hyperintensity (WMH) measured by magnetic resonance imaging (MRI).

resultsCSF SNAP-25 and SNAP-25/Aβ42 were increased in patients with pMCI and AD compared with CN, and in pMCI and AD compared with sMCI. Cognitively normal subjects who progressed to MCI or AD during follow-up had increased SNAP-25/Aβ42 ratio compared with nonprogressors. CSF SNAP-25, especially SNAP-25/Aβ42, offers diagnostic utility for pMCI and AD. CSF SNAP-25 and SNAP-25/Aβ42 significantly predicted conversion from MCI to AD. In addition, elevated SNAP-25/Aβ42 ratio was associated with the rate of hippocampal atrophy in pMCI and the rate of change of cognitive impairment in CN over the follow-up period.

conclusionsThese data suggest that both CSF SNAP-25 and SNAP-25/Aβ42 ratio are already increased at the early clinical stage of AD, and indicate the promise of CSF SNAP-25 and SNAP-25/Aβ42 ratio as diagnostic and prognostic biomarkers for the earliest symptomatic stage of AD.

Indexed as

AgedAged, 80 and overAlzheimer DiseaseAmyloid beta-PeptidesBrainCognitive DysfunctionFemaleHumansMagnetic Resonance ImagingMaleMental Status ScheduleMiddle AgedNerve DegenerationNeuropsychological TestsPeptide FragmentsPositron-Emission TomographyAmyloid beta-Peptidesamyloid beta-protein (1-42)Peptide FragmentsSNAP25 protein, humanSynaptosomal-Associated Protein 25Alzheimer’s diseaseAmyloid-βSynaptic lossSynaptosomal-associated protein 25

Identifiers

PMID30115118
PMCPMC6097333
OpenAlexW2887353432

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.