Evidence map›Paper›PMID 31749651›Full record

ReviewDialogues in clinical neuroscience2019

The synaptic pathology of cognitive life
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William G Honer, Alfredo Ramos-Miguel, Jehan Alamri, Ken Sawada, Alasdair M Barr, Julie A Schneider, David A Bennett

Abstract readReview
In one paragraph

Review in Dialogues in clinical neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Late-life physical activity relates to brain tissue synaptic integrity markers in older adults.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2022
    Article
  10. Article
  11. Room for Two: The Synaptophysin/Synaptobrevin Complex.Frontiers in synaptic neuroscience · 2021
    Article
  12. Article
  13. CaCells · 2020
    Review
  14. 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

7 authors.

William G HonerDepartments of Psychiatry, University of British Columbia, Vancouver, British Columbia, Canada.
Alfredo Ramos-MiguelDepartment of Pharmacology, University of the Basque Country, and Centro de Investigación Biomédica en Red de Salud Mental, CIBERSAM, Madrid, Spain.
Jehan AlamriDepartments of Anaesthesia, Pharmacology & Therapeutics, University of British Columbia, Vancouver, British Columbia, Canada.
Ken SawadaKochi Medical School, Kochi, Japan.
Alasdair M BarrDepartments of Anaesthesia, Pharmacology & Therapeutics, University of British Columbia, Vancouver, British Columbia, Canada.
Julie A SchneiderRush Alzheimer's Disease Center, Rush University Medical Center, Chicago, US.
David A BennettRush Alzheimer's Disease Center, Rush University Medical Center, Chicago, US.

Funding

EPIDEMIOLOGY OF NEURAL RESERVE AND NEUROBIOLOGY IN AGINGR01AG017917 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI BENNETT, DAVID ALAN · 2001 to 2023
$43.3M
Epidemiologic Study of TDP-43 Pathology in Aging and DementiaR01AG042210 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI SCHNEIDER, JULIE A. · 2012 to 2018
$2.4M
CIHR MOP-81112CIHR MT-14037NIA NIH HHS R01 AG017917NIA NIH HHS R01 AG042210
6 · The paper itself

Abstract

Prospective, community-based studies allow evaluation of associations between cognitive functioning and synaptic measures, controlled for age-related pathologies. Findings from >400 community-based participants are reviewed. Levels of two presynaptic proteins, complexin-I (inhibitory terminals), and complexin-II (excitatory terminals) contributed to cognitive variation from normal to dementia. Adding the amount of protein-protein interaction between two others, synaptosome-associated protein-25 and syntaxin, explained 6% of overall variance. The presynaptic protein Munc18-1 long variant was localized to inhibitory terminals, and like complexin-I, was positively associated with cognition. Associations depended on Braak stage, with the level of complexin-I contributing nearly 15% to cognitive variation in stages 0-II, while complexin-II contributed 7% in stages V-VI. Non-denaturing gels identified multiple soluble N-ethylmaleimide-sensitive factor attachment protein receptor protein-protein (SNARE) complexes in frontal and in temporal lobes, making specific contributions to cognitive functions. Multiple mechanisms of presynaptic plasticity contribute to cognitive function during aging.
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Indexed as

AgingAnimalsCognitionCognitive DysfunctionHumansProspective StudiesSNARE ProteinsSynapsesSNARE ProteinsagingAlzheimer diseasecognitive declinecomplexinexcitatory/inhibitory 
balanceMunc18SNAP-25SNARE complexsynaptic pathologysyntaxin

Identifiers

PMID31749651
PMCPMC6829169

What OpenQuestion holds

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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.