Neuronal Deposition of Amyloid-β Oligomers and Hyperphosphorylated Tau Is Closely Connected with Cognitive Dysfunction in Aged Dogs.
Alzheimer’s disease
Aβ1 - 42 oligomers
amyloid-β plaques
canine cognitive dysfunction
hyperphosphorylated tau
Journal
Journal of Alzheimer's disease reports
ISSN: 2542-4823
Titre abrégé: J Alzheimers Dis Rep
Pays: Netherlands
ID NLM: 101705500
Informations de publication
Date de publication:
2021
2021
Historique:
accepted:
30
08
2021
entrez:
6
12
2021
pubmed:
7
12
2021
medline:
7
12
2021
Statut:
epublish
Résumé
Canine 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. The 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. Immunohistochemical and immunofluorescence analysis of the cortical and hippocampal regions of five CCD-affected and two nondemented aged dogs using 4G8 anti-Aβp, anti-Aβ The 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 Taken 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.
Sections du résumé
BACKGROUND
BACKGROUND
Canine 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.
OBJECTIVE
OBJECTIVE
The 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.
METHODS
METHODS
Immunohistochemical and immunofluorescence analysis of the cortical and hippocampal regions of five CCD-affected and two nondemented aged dogs using 4G8 anti-Aβp, anti-Aβ
RESULTS
RESULTS
The 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
CONCLUSION
CONCLUSIONS
Taken 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.
Identifiants
pubmed: 34870101
doi: 10.3233/ADR-210035
pii: ADR210035
pmc: PMC8609497
doi:
Types de publication
Journal Article
Langues
eng
Pagination
749-760Informations de copyright
© 2021 – The authors. Published by IOS Press.
Déclaration de conflit d'intérêts
The authors have no conflict of interest to report.
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