ArticleJournal of Alzheimer's disease reports2021
Neuronal Deposition of Amyloid-β Oligomers and Hyperphosphorylated Tau Is Closely Connected with Cognitive Dysfunction in Aged Dogs.
Article in Journal of Alzheimer's disease reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
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Who cites it
5 citing papers in PubMed, 12 citations in OpenAlex.
- Higher burden of neuropsychiatric symptom-like behaviors associated with canine cognitive dysfunction compared to normal aging in the Dog Aging Project.GeroScience · 2026Article
- Advances in biomarker discovery for canine cognitive dysfunction: a comprehensive structured narrative review and future perspectives.Veterinary research communications · 2026Review
- The canine blood-brain barrier in health and disease: focus on brain protection.The veterinary quarterly · 2025Review
- Unveiling the significance of dog domestication in cognitive dysfunction: Are wolves protected?Open veterinary journal · 2025Article
- Alzheimer's Disease Neuropathological Change in Aged Non-Primate Mammals.International journal of molecular sciences · 2024Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCanine cognitive dysfunction (CCD) is a progressive syndrome recognized in mature to aged dogs with a variety of neuropathological changes similar to human Alzheimer's disease (AD), for which it is thought to be a good natural model. However, the presence of hyperphosphorylated tau protein (p-Tau) in dogs with CCD has only been demonstrated infrequently.
objectiveThe aim of the present study was to investigate the presence of p-Tau and amyloid-β oligomer (Aβo) in cerebral cortex and hippocampus of dogs with CCD, with focus on an epitope retrieval protocol to unmask p-Tau.
methodsImmunohistochemical and immunofluorescence analysis of the cortical and hippocampal regions of five CCD-affected and two nondemented aged dogs using 4G8 anti-Aβp, anti-Aβ
resultsThe extracellular Aβ senile plaques were of the diffuse type which lack the dense core normally seen in human AD. While p-Tau deposits displayed a widespread pattern and closely resembled the typical human neuropathology, they did not co-localize with the Aβp. Of considerable interest, however, widespread intraneuronal deposition of Aβ
conclusionTaken together, these findings reveal further shared neuropathologic features of AD and CCD, supporting the case that aged dogs afflicted with CCD offer a relevant model for investigating human AD.
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