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Cited by 53Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

Amyloid and tau pathology of familial Alzheimer’s disease APP/PS1 mouse model in a senescence phenotype background (SAMP8)

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Porquet, D., Andrés-Benito, P., Griñán-Ferré, C., Camins, A., Ferrer, I., Canudas, A. M., Del Valle, J., Pallàs, Mercè·2015·AGE
DOI 10.1007/s11357-015-9747-3PMC PMC4320125
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Abstract

The amyloid precursor protein/presenilin 1 (APP/PS1) mouse model of Alzheimer's disease (AD) has provided robust neuropathological hallmarks of familial AD-like pattern at early ages, whereas senescence-accelerated mouse prone 8 (SAMP8) has a remarkable early senescence phenotype with pathological similarities to AD. The aim of this study was the investigation and characterization of cognitive and neuropathological AD markers in a novel mouse model that combines the characteristics of the APP/PS1 transgenic mouse model with a senescence-accelerated background of SAMP8 mice. Initially, significant differences were found regarding amyloid plaque formation and cognitive abnormalities. Bearing these facts in mind, we determined a general characterization of the main AD brain molecular markers, such as alterations in amyloid pathway, neuroinflammation, and hyperphosphorylation of tau in these mice along their lifetimes. Results from this analysis revealed that APP/PS1 in SAMP8 background mice showed alterations in the pathways studied in comparison with SAMP8 and APP/PS1, demonstrating that a senescence-accelerated background exacerbated the amyloid pathology and maintained the cognitive dysfunction present in APP/PS1 mice. Changes in tau pathology, including the activity of cyclin-dependent kinase 5 (CDK5) and glycogen synthase kinase 3 β (GSK3β), differs, but not in a parallel manner, with amyloid disturbances.

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  • Levels of pTau are not high in the APP/PS1 mouse model.

    “Levels of pTau are not high in the APP/PS1 mouse model [36]”

    From Microglia specific deletion of miR-155 in Alzheimer’s disease mouse models reduces amyloid-β pathology but causes hyperexcitability and seizures (2023) · cites this paper as [36]

    The Results (Characterization in tau pathology; Fig. 9, page unavailable) report higher phospho-tau levels in APP/PS1 mice than in SAMP8 mice at the oldest age tested. The Discussion specifies higher phosphorylation at three tau sites at 12 months, although it found no clear strain differences at earlier ages. The unqualified claim that pTau levels are not high in APP/PS1 mice conflicts with the reported finding at 12 months. (LLM, conf=0.88)

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Authors
Porquet, D., Andrés-Benito, P., Griñán-Ferré, C., Camins, A., Ferrer, I., Canudas, A. M., Del Valle, J., & Pallàs, M.
Affiliations
  • Institut de Biomedicina de la Universitat de Barcelona (ES)
  • Biomedical Research Networking Center on Neurodegenerative Diseases (ES)
  • Bellvitge University Hospital (ES)
Corresponding author
Pallàs, Mercè
ORCID
Venue
AGE
Publisher
Springer Science and Business Media LLC
Published
2015-02
Volume
37
Issue
1
Pages
9747-9747
ISSN
  • 0161-9152 (ISSN-L)
  • 1574-4647
DOI
10.1007/s11357-015-9747-3
PMC
PMC4320125
OpenAlex
W2071167787
Cited by
53
References
3
Citations by year
2026: 1 · 2025: 2 · 2024: 11 · 2023: 3 · 2022: 2 · 2021: 8 · 2020: 4 · 2019: 6 · 2018: 7 · 2017: 4 · 2016: 5
FWCI
3.93
Type
journal article
Language
en
Open access
Licence
www.springer.com/tdm (tdm)
Locations
  • AGE (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • RECERCAT (Consorci de Serveis Universitaris de Catalunya) (acceptedVersion)
  • Dipòsit Digital de la Universitat de Barcelona (Universitat de Barcelona) (submittedVersion, public-domain)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
Alzheimer's disease, APP/PS1 mice, SAMP8 mice, senescence-accelerated mice, amyloid plaques, tau hyperphosphorylation, neuroinflammation, cognitive impairment, cyclin-dependent kinase 5, glycogen synthase kinase-3β, familial Alzheimer's disease, amyloid precursor protein, presenilin 1, mouse model
MeSH terms
Aging, Alzheimer Disease, Animals, Disease Models, Animal, Mice, Transgenic, Phenotype, Amyloid beta-Protein Precursor, tau Proteins, Mice, Presenilin-1

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