Evidence map›Paper›PMID 40799280›Full record

ReviewBrain communications2025

Spontaneous mammalian models for Alzheimer's disease and dementia.

Madeleine Ford, Frank J Gunn-Moore, Mark P Dagleish

Abstract readReview
In one paragraph

Review in Brain communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Madeleine FordSchool of Biology, Biomedical Sciences Research Complex, University of St Andrews, St Andrews KY16 9ST, UK.
Frank J Gunn-MooreSchool of Biology, Biomedical Sciences Research Complex, University of St Andrews, St Andrews KY16 9ST, UK.
Mark P DagleishDivision of Veterinary Pathology, Public Health and Disease Investigation, School of Biodiversity, One Health and Veterinary Medicine, University of Glasgow, Glasgow G61 1QH, UK.ORCID https://orcid.org/0000-0001-6909-6467

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Globally, the human population is ageing, and, consequently, the prevalence of major neurocognitive disorders is increasing, resulting in a greater need for novel dementia therapeutic interventions. Animal models are invaluable in studying underlying pathological processes in human diseases and with evidence for rising life expectancy in many domesticated animals studies have investigated neurocognitive disorders in several non-human species. Rodents have been used extensively as animal models, but this review will examine published literature suggesting candidate non-laboratory animal models for studying dementia, especially human Alzheimer's disease. Comparison of the physiological, pathological and clinical features of companion animals, farm animals and marine mammals shows that although many animals develop amyloid plaques and, to lesser degree, hyperphosphorylated tau protein, very few develop neurofibrillary tangles or neuronal loss to the same extent as humans with Alzheimer's disease. Several hypotheses are proposed as to why, as yet, no animals have been found to spontaneously develop Alzheimer's disease-like pathology to the same level as humans but highlight specific aspects where these models may be useful if developed further.

Indexed as

Alzheimer’s diseasemammalianmodelsnon-laboratory

Identifiers

PMID40799280
PMCPMC12343051

What OpenQuestion holds

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LicenceCC BY
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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.