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Cited by 177Alzheimer's disease research and treatmentsCell death mechanisms and regulationNeuroinflammation and Neurodegeneration Mechanisms

Tumor Necrosis Factor Death Receptor Signaling Cascade Is Required for Amyloid-β Protein-Induced Neuron Death

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Li, Rena, Yang, Libang, Lindholm, Kristina, Konishi, Yoshihiro, Yue, Xu, Hampel, Harald, Zhang, Dai, Shen, Yong·2004·The Journal of Neuroscience
DOI 10.1523/jneurosci.4580-03.2004PMC PMC6730458
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Abstract

Tumor necrosis factor type I receptor (TNFRI), a death receptor, mediates apoptosis and plays a crucial role in the interaction between the nervous and immune systems. A direct link between death receptor activation and signal cascade-mediated neuron death in brains with neurodegenerative disorders remains inconclusive. Here, we show that amyloid-β protein (Aβ), a major component of plaques in the Alzheimer's diseased brain, induces neuronal apoptosis through TNFRI by using primary neurons overexpressing TNFRI by viral infection or neurons from TNFRI knock-out mice. This was mediated via alteration of apoptotic protease-activating factor (Apaf-1) expression that in turn induced activation of nuclear factor κB (NF-κB). Aβ-induced neuronal apoptosis was reduced with lower Apaf-1 expression, and little NF-κB activation was found in the neurons with mutated Apaf-1 or a deletion of TNFRI compared with the cells from wild-type (WT) mice. Our studies suggest a novel neuronal response of Aβ, which occurs through a TNF receptor signaling cascade and a caspase-dependent death pathway.

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  • Aβ is capable of binding to TNFR1, which ultimately leads to activation of NF-kB and neuronal apoptosis.

    “Aβ is capable of binding to TNFR1 which ultimately leads to activation of NF-kB and neuronal apoptosis [147].”

    From Glial contributions to neurodegeneration in tauopathies (2017) · cites this paper as [147]

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Authors
Li, R., Yang, L., Lindholm, K., Konishi, Y., Yue, X., Hampel, H., Zhang, D., & Shen, Y.
Affiliations
  • Banner Sun Health Research Institute (US)
  • Oregon Health & Science University (US)
  • Ehime University (JP)
  • Ludwig-Maximilians-Universität München (DE)
  • Peking University (CN)
  • Arizona State University (US)
ORCID
Venue
The Journal of Neuroscience
Publisher
Society for Neuroscience
Published
2004-02-18
Volume
24
Issue
7
Pages
1760-1771
ISSN
  • 0270-6474 (ISSN-L)
  • 1529-2401
DOI
10.1523/jneurosci.4580-03.2004
PMC
PMC6730458
OpenAlex
W2067712423
Cited by
177
References
3
Citations by year
2026: 3 · 2025: 6 · 2024: 6 · 2023: 6 · 2022: 6 · 2021: 5 · 2020: 8 · 2019: 6 · 2018: 7 · 2017: 8 · 2016: 6 · 2015: 8 · 2014: 5 · 2013: 9 · 2012: 18
FWCI
6.47
Type
journal article
Language
en
Open access
Licence
Locations
Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
death receptor signaling, amyloid-beta, neuronal apoptosis, Apaf-1, NF-κB activation, caspase-dependent cell death, Alzheimer's disease, neurodegeneration

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