Evidence map›Paper›PMID 36547260›Full record

ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2023

Synaptic resilience is associated with maintained cognition during ageing.

Declan King, Kris Holt, Jamie Toombs, Xin He, Owen Dando, Judith A Okely, Makis Tzioras, Jamie Rose, Ciaran Gunn, Adele Correia and 12 more

Open access · hybridAbstract read
In one paragraph

Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
3.7field-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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

  1. Systematic review and meta-analysis of bulk RNAseq studies in human Alzheimer's disease brain tissue.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Pooled it
  2. Trial
  3. Article
  4. Article
  5. Direct evidence for dendritic spine compensation and regeneration in Alzheimer's disease models.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Lessons we learned from the Lothian Birth Cohorts of 1921 and 1936.Genomic psychiatry : advancing science from genes to society · 2025
    Article
  13. Article
  14. Article
  15. Synaptic gene expression changes in frontotemporal dementia due to themedRxiv : the preprint server for health sciences · 2024
    Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Synaptic Compensatory Plasticity in Alzheimer's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    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

22 authors at 4 institutions in 1 country.

Declan KingUK Dementia Research Institute and Centre for Discovery Brain Sciences at the University of Edinburgh, Edinburgh, UK.
Kris HoltUK Dementia Research Institute and Centre for Discovery Brain Sciences at the University of Edinburgh, Edinburgh, UK.
Jamie ToombsUK Dementia Research Institute and Centre for Discovery Brain Sciences at the University of Edinburgh, Edinburgh, UK.
Xin HeUK Dementia Research Institute and Centre for Discovery Brain Sciences at the University of Edinburgh, Edinburgh, UK.
Owen DandoUK Dementia Research Institute and Centre for Discovery Brain Sciences at the University of Edinburgh, Edinburgh, UK.
Judith A OkelyLothian Birth Cohorts, Department of Psychology, University of Edinburgh, Edinburgh, UK.
Makis TziorasUK Dementia Research Institute and Centre for Discovery Brain Sciences at the University of Edinburgh, Edinburgh, UK.
Jamie RoseUK Dementia Research Institute and Centre for Discovery Brain Sciences at the University of Edinburgh, Edinburgh, UK.
Ciaran GunnUK Dementia Research Institute and Centre for Discovery Brain Sciences at the University of Edinburgh, Edinburgh, UK.
Adele CorreiaUK Dementia Research Institute and Centre for Discovery Brain Sciences at the University of Edinburgh, Edinburgh, UK.
Carmen MonteroUK Dementia Research Institute and Centre for Discovery Brain Sciences at the University of Edinburgh, Edinburgh, UK.
Hannah McAlisterUK Dementia Research Institute and Centre for Discovery Brain Sciences at the University of Edinburgh, Edinburgh, UK.
Jane TullochUK Dementia Research Institute and Centre for Discovery Brain Sciences at the University of Edinburgh, Edinburgh, UK.
Douglas LamontFingerPrints Proteomics Facility, School of Life Sciences, University of Dundee, Dundee, UK.
Adele M TaylorLothian Birth Cohorts, Department of Psychology, University of Edinburgh, Edinburgh, UK.
Sarah E HarrisLothian Birth Cohorts, Department of Psychology, University of Edinburgh, Edinburgh, UK.
Paul RedmondLothian Birth Cohorts, Department of Psychology, University of Edinburgh, Edinburgh, UK.
Simon R CoxLothian Birth Cohorts, Department of Psychology, University of Edinburgh, Edinburgh, UK.
Christopher M HenstridgeSystems Medicine, School of Medicine, University of Dundee, Dundee, UK.
Ian J DearyLothian Birth Cohorts, Department of Psychology, University of Edinburgh, Edinburgh, UK.
Colin SmithNeuropathology, Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, UK.
Tara L Spires-JonesUK Dementia Research Institute and Centre for Discovery Brain Sciences at the University of Edinburgh, Edinburgh, UK.
University of Edinburgh · GBUK Dementia Research Institute · GBUniversity of Dundee · GBNHS Lothian · GB

Funding

Biotechnology and Biological Sciences Research Council BB/W008793/1Medical Research Council MR/M01311/1Medical Research Council MR/R024065/1Wellcome TrustWellcome Trust 221890/Z/20/Z
6 · The paper itself

Abstract

introductionIt remains unclear why age increases risk of Alzheimer's disease and why some people experience age-related cognitive decline in the absence of dementia. Here we test the hypothesis that resilience to molecular changes in synapses contribute to healthy cognitive ageing.

methodsWe examined post-mortem brain tissue from people in mid-life (n = 15), healthy ageing with either maintained cognition (n = 9) or lifetime cognitive decline (n = 8), and Alzheimer's disease (n = 13). Synapses were examined with high resolution imaging, proteomics, and RNA sequencing. Stem cell-derived neurons were challenged with Alzheimer's brain homogenate.

resultsSynaptic pathology increased, and expression of genes involved in synaptic signaling decreased between mid-life, healthy ageing and Alzheimer's. In contrast, brain tissue and neurons from people with maintained cognition during ageing exhibited decreases in synaptic signaling genes compared to people with cognitive decline. DISCUSSION: Efficient synaptic networks without pathological protein accumulation may contribute to maintained cognition during ageing.

Indexed as

Alzheimer DiseaseCognitive AgingHealthy AgingSynapsesAdultAgedAged, 80 and overBrainCognitionCognitive DysfunctionFemaleGliosisHumansMaleMiddle AgedNeural Stem CellsageingAlzheimer'scognitionsynapse

Identifiers

PMID36547260
PMCPMC11497288
OpenAlexW4313277720

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.