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Increased NF-κB signalling up-regulates BACE1 expression and its therapeutic potential in Alzheimer's disease
Open accessAbstract
Elevated levels of β-site APP cleaving enzyme 1 (BACE1) were found in the brain of some sporadic Alzheimer's disease (AD) patients; however, the underlying mechanism is unknown. BACE1 cleaves β-amyloid precursor protein (APP) to generate amyloid β protein (Aβ), a central component of neuritic plaques in AD brains. Nuclear factor-kappa B (NF-κB) signalling plays an important role in gene regulation and is implicated in inflammation, oxidative stress and apoptosis. In this report we found that both BACE1 and NF-κB p65 levels were significantly increased in the brains of AD patients. Two functional NF-κB-binding elements were identified in the human BACE1 promoter region. We found that NF-κB p65 expression resulted in increased BACE1 promoter activity and BACE1 transcription, while disruption of NF-κB p65 decreased BACE1 gene expression in p65 knockout (RelA-knockout) cells. In addition, NF-κB p65 expression leads to up-regulated β-secretase cleavage and Aβ production, while non-steroidal anti-inflammatory drugs (NSAIDs) inhibited BACE1 transcriptional activation induced by strong NF-κB activator tumour necrosis factor-alpha (TNF-α). Taken together, our results clearly demonstrate that NF-κB signalling facilitates BACE1 gene expression and APP processing, and increased BACE1 expression mediated by NF-κB signalling in the brain could be one of the novel molecular mechanisms underlying the development of AD in some sporadic cases. Furthermore, NSAIDs could block the inflammation-induced BACE1 transcription and Aβ production. Our study suggests that inhibition of NF-κB-mediated BACE1 expression may be a valuable drug target for AD therapy.
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“Furthermore, treatment with non‐steroidal anti‐inflammatory drugs (NSAIDs) was found to decrease BACE1 transcription and subsequent production of Aβ.”
From BACE1: More than just a β‐secretase (2022) · cites this paper as [152]
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“The BACE1 promotor has an NFκB binding site. When phosphorylated, NFκB increases BACE1 promotor activity and transcription.”
From BACE1: More than just a β‐secretase (2022) · cites this paper as [152]
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“Moreover, it has also been proposed as a molecular factor underlying some sporadic forms of AD (Chen et al., 2012).”
From Exploring the Therapeutic Potential of Phytochemicals in Alzheimer’s Disease: Focus on Polyphenols and Monoterpenes (2022) · cites this paper as Chen et al., 2012
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Metadata
- Authors
- Chen, C.-H., Zhou, W., Liu, S., Deng, Y., Cai, F., Tone, M., Tone, Y., Tong, Y., & Song, W.
- Affiliations
- University of British Columbia (CA)
- University of Pennsylvania (US)
- Corresponding author
- Song, Weihong
- Venue
- The International Journal of Neuropsychopharmacology
- Publisher
- Oxford University Press (OUP)
- Published
- 2011-02-18
- Volume
- 15
- Issue
- 01
- Pages
- 77-90
- ISSN
- 1461-1457 (ISSN-L)
- 1469-5111
- OpenAlex
- W2158215064
- Cited by
- 433
- References
- 41
- Citations by year
- 2026: 33 · 2025: 55 · 2024: 51 · 2023: 39 · 2022: 40 · 2021: 26 · 2020: 47 · 2019: 25 · 2018: 25 · 2017: 18 · 2016: 20 · 2015: 17 · 2014: 12 · 2013: 11 · 2012: 6
- FWCI
- 7.85
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The International Journal of Neuropsychopharmacology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Michael Smith Health Research BC
- Canada Research Chairs
- Canadian Institutes of Health Research
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, BACE1, NF-κB signaling, NF-κB p65, beta-secretase, amyloid-beta production, APP processing, transcriptional regulation, nonsteroidal anti-inflammatory drugs, TNF-α, inflammation, therapeutic target
- MeSH terms
- Aged, Aged, 80 and over, Alzheimer Disease, Anti-Inflammatory Agents, Non-Steroidal, Brain, Humans, Promoter Regions, Genetic, Transcription, Genetic, Tumor Necrosis Factor-alpha, Signal Transduction, Up-Regulation, Amyloid beta-Peptides, Aspartic Acid Endopeptidases, Amyloid beta-Protein Precursor, Transcription Factor RelA, Amyloid Precursor Protein Secretases
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