Evidence map›Paper›PMID 26651821›Full record

ArticleActa neuropathologica communications2015

The domestic cat as a natural animal model of Alzheimer's disease.

James K Chambers, Takahiko Tokuda, Kazuyuki Uchida, Ryotaro Ishii, Harutsugu Tatebe, Erika Takahashi, Takami Tomiyama, Yumi Une, Hiroyuki Nakayama

Open access · goldAbstract read
In one paragraph

Article in Acta neuropathologica communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

50 citing papers in PubMed, 89 citations in OpenAlex.

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  4. From Circuits to Lifespan: Translating Mouse and Human Timelines with Neuroimaging-Based Tractography.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
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  5. Review
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  7. Amyloid-Beta, Tau, and Microglial Activation in Aged Felid Brains.The Journal of comparative neurology · 2024
    Article
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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

9 authors at 4 institutions in 1 country.

James K ChambersDepartment of Veterinary Pathology, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Tokyo, Japan.
Takahiko TokudaDepartment of Molecular Pathobiology of Brain Diseases, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Kazuyuki UchidaDepartment of Veterinary Pathology, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Tokyo, Japan. auchidak@mail.ecc.u-tokyo.ac.jp.
Ryotaro IshiiDepartment of Neurology, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Harutsugu TatebeDepartment of Neurology, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Erika TakahashiLaboratory of Veterinary Pathology, School of Veterinary Medicine, Azabu University, Kanagawa, Japan.
Takami TomiyamaDepartment of Neuroscience, Osaka City University Graduate School of Medicine, Osaka, Japan. tomi@med.osaka-cu.ac.jp.
Yumi UneLaboratory of Veterinary Pathology, School of Veterinary Medicine, Azabu University, Kanagawa, Japan.
Hiroyuki NakayamaDepartment of Veterinary Pathology, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Tokyo, Japan.
Kyoto Prefectural University of Medicine · JPThe University of Tokyo · JPAzabu University · JPOsaka City University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionAlzheimer's disease (AD) is the most dominant neurodegenerative disorder that causes dementia, and no effective treatments are available. To study its pathogenesis and develop therapeutics, animal models representing its pathologies are needed. Although many animal species develop senile plaques (SP) composed of amyloid-β (Aβ) proteins that are identical to those found in humans, none of them exhibit neurofibrillary tangles (NFT) and subsequent neurodegeneration, which are integral parts of the pathology of AD.

resultsThe present study shows that Aβ accumulation, NFT formation, and significant neuronal loss all emerge naturally in the hippocampi of aged domestic cats. The NFT that form in the cat brain are identical to those seen in human AD in terms of their spatial distribution, the cells they affect, and the tau isoforms that comprise them. Interestingly, aged cats do not develop mature argyrophilic SP, but instead accumulate intraneuronal Aβ oligomers in their hippocampal pyramidal cells, which might be due to the amino acid sequence of felid Aβ.

conclusionsThese results suggest that Aβ oligomers are more important than SP for NFT formation and the subsequent neurodegeneration. The domestic cat is a unique animal species that naturally replicates various AD pathologies, especially Aβ oligomer accumulation, NFT formation, and neuronal loss.

Indexed as

Disease Models, AnimalAgingAmyloid beta-PeptidesAnimalsBrainCatsEmbryo, MammalianFemaleHumansMaleMicroscopy, Electron, TransmissionNerve Tissue ProteinsNeurofibrillary TanglesNeuronstau ProteinsAmyloid beta-PeptidesNerve Tissue Proteinstau Proteins

Identifiers

PMID26651821
PMCPMC4674944
OpenAlexW2217253827

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.