Cited by 435Alzheimer's disease research and treatmentsNF-κB Signaling PathwaysNeuroinflammation and Neurodegeneration Mechanisms

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Increased NF-κB signalling up-regulates BACE1 expression and its therapeutic potential in Alzheimer's disease

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Chen, Chia-Hsiung, Zhou, Weihui, Liu, Shengchun, Deng, Yu, Cai, Fang, Tone, Masahide, Tone, Yukiko, Tong, Yigang, Song, Weihong·2012·The International Journal of Neuropsychopharmacology

DOI 10.1017/s1461145711000149

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Abstract

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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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
ORCID: Zhou, Weihui
Liu, Shengchun
Deng, Yu
Cai, Fang
Tong, Yigang
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
DOI: 10.1017/s1461145711000149
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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Increased NF-κB signalling up-regulates BACE1 expression and its therapeutic potential in Alzheimer's disease

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