Evidence map›Paper›PMID 36514861›Full record

ArticleThe European journal of neuroscience2023

Alzheimer's disease-like neuropathology in three species of oceanic dolphin.

Marissa C Vacher, Claire S Durrant, Jamie Rose, Ailsa J Hall, Tara L Spires-Jones, Frank Gunn-Moore, Mark P Dagleish

Open access · hybridAbstract read
In one paragraph

Article in The European journal of neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 2 pooled it
4.9field-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

19 citing papers in PubMed, 2 syntheses or guidelines pooled it, 30 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. The neuromodulatory fragility hypothesis of Alzheimer's disease pathogenesis.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  4. Astrocyte properties in cetacean cortices.Physiological reports · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Meningeal Lymphatic and Glymphatic Structures in a Pelagic Delphinid (Animals : an open access journal from MDPI · 2025
    Article
  12. Review
  13. Review
  14. Alzheimer's Disease Neuropathological Change in Aged Non-Primate Mammals.International journal of molecular sciences · 2024
    Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. 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

7 authors at 5 institutions in 3 countries.

Marissa C VacherInstitute of Biology, Leiden University, Leiden, the Netherlands.
Claire S DurrantCentre for Discovery Brain Sciences and UK Dementia Research Institute, University of Edinburgh, Edinburgh, UK.ORCID 0000-0001-7552-7358
Jamie RoseCentre for Discovery Brain Sciences and UK Dementia Research Institute, University of Edinburgh, Edinburgh, UK.
Ailsa J HallSea Mammal Research Unit, Scottish Oceans Institute, University of St. Andrews, Fife, UK.
Tara L Spires-JonesCentre for Discovery Brain Sciences and UK Dementia Research Institute, University of Edinburgh, Edinburgh, UK.ORCID 0000-0003-2530-0598
Frank Gunn-MooreSchool of Biology, University of St Andrews, Fife, UK.
Mark P DagleishSchool of Biodiversity, One Health and Veterinary Medicine, Pathology Department, University of Glasgow, Scotland, UK.
UK Dementia Research Institute · GBAndrews University · USLeiden University · NLUniversity of Glasgow · GBUniversity of St Andrews · GB

Funding

European Research Council 681181UK Medical Research Council
6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most common neurodegenerative disease and the primary cause of disability and dependency among elderly humans worldwide. AD is thought to be a disease unique to humans although several other animals develop some aspects of AD-like pathology. Odontocetes (toothed whales) share traits with humans that suggest they may be susceptible to AD. The brains of 22 stranded odontocetes of five different species were examined using immunohistochemistry to investigate the presence or absence of neuropathological hallmarks of AD: amyloid-beta plaques, phospho-tau accumulation and gliosis. Immunohistochemistry revealed that all aged animals accumulated amyloid plaque pathology. In three animals of three different species of odontocete, there was co-occurrence of amyloid-beta plaques, intraneuronal accumulation of hyperphosphorylated tau, neuropil threads and neuritic plaques. One animal showed well-developed neuropil threads, phospho-tau accumulation and neuritic plaques, but no amyloid plaques. Microglia and astrocytes were present as expected in all brain samples examined, but we observed differences in cell morphology and numbers between individual animals. The simultaneous occurrence of amyloid-beta plaques and hyperphosphorylated tau pathology in the brains of odontocetes shows that these three species develop AD-like neuropathology spontaneously. The significance of this pathology with respect to the health and, ultimately, death of the animals remains to be determined. However, it may contribute to the cause(s) of unexplained live-stranding in some odontocete species and supports the 'sick-leader' theory whereby healthy conspecifics in a pod mass strand due to high social cohesion.

Indexed as

Alzheimer DiseaseDolphinsNeurodegenerative DiseasesAgedAmyloid beta-PeptidesAnimalsBrainHumansNeurofibrillary TanglesPlaque, Amyloidtau ProteinsAmyloid beta-Peptidestau Proteinsamyloid plaquesbeta amyloidcetaceanimmunohistochemistryneurofibrillary tanglesodontocetestau

Identifiers

PMID36514861
PMCPMC10947196
OpenAlexW4311494424

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.