Inhibition of Aβ production by NF-κB inhibitors
Abstract
The transcription factor nuclear factor kappaB (NF-kappaB) is widely expressed in the nervous system and increased NF-kappaB immunoreactivity has been observed in Alzheimer's disease (AD) brains in the nuclei of neurons within the vicinity of diffuse beta-amyloid plaques. Beta-amyloid (Abeta) peptides are the main constituent of senile plaques and are known to stimulate NF-kappaB activity. In the present study, we investigated the effect of various NF-kappaB inhibitors on the production of Abeta1-40, Abeta1-42, secreted APP (sAPPbeta and sAPPalpha) and APP C-terminal fragments (APP-CTF) using CHO cells overexpressing the beta-amyloid precursor protein (APP). Our data show that NF-kappaB inhibitors decrease both Abeta1-40 and Abeta1-42 production. In addition, we show that some NF-kappaB inhibitors decrease sAPPbeta and APP-CTFbeta suggesting that they reduce the beta-secretase cleavage of APP. Altogether our data suggest that NF-kappaB inhibitors may be of therapeutic importance for the treatment of AD pathology not only by blocking inflammatory processes but also by directly inhibiting the production of Abeta peptides.
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NF-κB could be under the control of PKR in Alzheimer's disease because NF-κB is activated in Alzheimer's disease.
“However, NF-κB could be under the control of PKR in AD because this factor is activated in AD [177, 178].”
From PKR, the double stranded RNA‐dependent protein kinase as a critical target in Alzheimer's disease (2009) · cites this paper as [178]
Cites
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Role of TGFβ signaling in the pathogenesis of Alzheimer’s disease
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PKR, the double stranded RNA‐dependent protein kinase as a critical target in Alzheimer's disease
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- Authors
- Paris, D., Patel, N., Quadros, A., Linan, M., Bakshi, P., Ait-Ghezala, G., & Mullan, M.
- Affiliations
- Roskamp Institute (US)
- Corresponding author
- Paris, Daniel
- Venue
- Neuroscience Letters
- Publisher
- Elsevier BV
- Published
- 2007-03
- Volume
- 415
- Issue
- 1
- Pages
- 11-16
- ISSN
- 0304-3940 (ISSN-L)
- OpenAlex
- W1971497818
- Cited by
- 75
- References
- 1
- Citations by year
- 2026: 3 · 2024: 3 · 2020: 2 · 2019: 4 · 2018: 1 · 2017: 3 · 2016: 5 · 2015: 11 · 2014: 8 · 2013: 4 · 2012: 5
- FWCI
- 3.51
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuroscience Letters (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Keywords
- NF-κB inhibitors, amyloid-beta production, Alzheimer's disease, APP processing, APP C-terminal fragments, Aβ40, amyloid-beta 42, amyloid plaques, neuroinflammation, therapeutic target
- MeSH terms
- Alzheimer Disease, Animals, Brain, Cricetulus, Dose-Response Relationship, Drug, Enzyme Inhibitors, Cricetinae, Humans, Peptide Fragments, Peptides, Protein Synthesis Inhibitors, Transcriptional Activation, Down-Regulation, Amyloid beta-Peptides, NF-kappa B, CHO Cells, Amyloid beta-Protein Precursor, Neuroprotective Agents, Amyloid Precursor Protein Secretases, Plaque, Amyloid
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