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Cited by 32Alzheimer's disease research and treatmentsPI3K/AKT/mTOR signaling in cancerProtein Kinase Regulation and GTPase Signaling

Dissociation of Akt/PKB and ribosomal S6 kinase signaling markers in a transgenic mouse model of Alzheimer’s disease

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Damjanac, Milena, Rioux Bilan, Agnès, Paccalin, Marc, Pontcharraud, Raymond, Fauconneau, Bernard, Hugon, Jacques, Page, Guylène·2008·Neurobiology of Disease
DOI 10.1016/j.nbd.2007.09.008
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Abstract

Previous studies demonstrated that the PKR (double-stranded RNA-activated protein kinase) pathway was activated while the mTOR (mammalian target of rapamycin) pathway was inhibited in Alzheimer's disease (AD). Here, we analysed upstream and downstream factors of mTOR in brain of APP(SL)/PS1 KI mice displaying a massive neuronal loss in hippocampus. While mTOR levels were not modified, we found a great activation of Akt with a robust accumulation of P-Akt((T308)) in non-apoptotic neurons at 6 months of age. At the opposite, a significant decrease of the p70/85S6K activation was observed in brain of PS1 KI and APP(SL)/PS1 KI mice with a very weak or no nucleocytoplasmic P-p70/85S6K((T389)) staining in apoptotic neurons of APP(SL)/PS1 KI mice. Furthermore, the activation of Erk1/2, 4E-BP1 and p70S6K((T421/S424)) (substrate of Erk1/2), except eIF4E, was not modified. These findings demonstrate a clear dissociation between Akt and ribosomal S6K signaling markers in these mice which could be involved in the AD pathological process.

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Crossref · 10.1016/j.nbd.2007.09.008

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  • There are two different neuronal responses: some neurons are characterized by a highly reactive Akt/mTOR/RS6K signalling pathway involved in τ-hyperphosphorylation and in future NFTs, and other neurons display a total inhibition of PT389-p70/85S6K leading to the apoptotic process in AD.

    “Taken together, one may propose that there are two different neuronal responses: some neurons are characterized by a highly reactive Akt/mTOR/RS6K signalling pathway involved in τ-hyperphospho-rylation and in future NFTs and other neurons displayed a total inhibition of PT389-p70/85S6K leading to the apoptotic process in AD [91, 94].”

    From PKR, the double stranded RNA‐dependent protein kinase as a critical target in Alzheimer's disease (2009) · cites this paper as [91]

  • These findings demonstrate a clear dissociation between Akt and ribosomal S6K signalling markers in these mice.

    “These findings demonstrate a clear dissociation between Akt and ribosomal S6K signalling markers in these mice which could be involved in the AD pathological process [91].”

    From PKR, the double stranded RNA‐dependent protein kinase as a critical target in Alzheimer's disease (2009) · cites this paper as [91]

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Authors
Damjanac, M., Rioux Bilan, A., Paccalin, M., Pontcharraud, R., Fauconneau, B., Hugon, J., & Page, G.
Affiliations
  • Université de Poitiers (FR)
  • Université Paris Cité (FR)
Corresponding author
Page, Guylène
ORCID
Venue
Neurobiology of Disease
Publisher
Elsevier BV
Published
2008-02
Volume
29
Issue
2
Pages
354-367
ISSN
0969-9961 (ISSN-L)
DOI
10.1016/j.nbd.2007.09.008
OpenAlex
W1966759047
Cited by
32
References
5
Citations by year
2025: 2 · 2024: 1 · 2023: 1 · 2021: 1 · 2020: 2 · 2019: 1 · 2017: 3 · 2016: 2 · 2015: 2 · 2014: 2 · 2013: 1 · 2012: 2
FWCI
2.67
Type
journal article
Language
en
Open access
Licence
Locations
  • Neurobiology of Disease (publishedVersion)
  • PubMed (publishedVersion)
  • HAL (submittedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
Centre Hospitalier Universitaire de Poitiers
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
Keywords
Alzheimer's disease, Akt signaling, RSK, mTOR signaling, APP/PS1 mice, neuronal apoptosis, hippocampus, ERK1/2, 4E-BP1, eIF4E
MeSH terms
Age Factors, Alzheimer Disease, Animals, Brain, Disease Models, Animal, Mice, Transgenic, Nerve Tissue Proteins, Signal Transduction, Gene Expression Regulation, Enzymologic, Amyloid beta-Protein Precursor, Ribosomal Protein S6 Kinases, In Situ Nick-End Labeling, Oncogene Protein v-akt, Mice, Presenilin-1

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