PreprintCited by 392NF-κB Signaling PathwaysNeuroinflammation and Neurodegeneration MechanismsNeuroscience and Neuropharmacology Research

NF- B in the Nervous System

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Kaltschmidt, B., Kaltschmidt, C.·2009·Cold Spring Harbor Perspectives in Biology

Abstract

The transcription factor NF-kappaB has diverse functions in the nervous system, depending on the cellular context. NF-kappaB is constitutively activated in glutamatergic neurons. Knockout of p65 or inhibition of neuronal NF-kappaB by super-repressor IkappaB resulted in the loss of neuroprotection and defects in learning and memory. Similarly, p50-/- mice have a lower learning ability and are sensitive to neurotoxins. Activated NF-kappaB can be transported retrogradely from activated synapses to the nucleus to translate short-term processes to long-term changes such as axon growth, which is important for long-term memory. In glia, NF-kappaB is inducible and regulates inflammatory processes that exacerbate diseases such as autoimmune encephalomyelitis, ischemia, and Alzheimer's disease. In summary, inhibition of NF-kappaB in glia might ameliorate disease, whereas activation in neurons might enhance memory. This review focuses on results produced by the analysis of genetic models.

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  • NF-kB is critical for homeostatic neuronal function.

    “These data suggest that on top of its function as a pro‐survival and pro‐inflammatory transcription factor, NF‐kB is also critical for homeostatic neuronal function (Kaltschmidt & Kaltschmidt, 2009).”

    From Mechanisms of DNA damage-mediated neurotoxicity in neurodegenerative disease (2022) · cites this paper as Kaltschmidt & Kaltschmidt, 2009

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References 78 · Cited by 392

Research works printed but not linked: 1

  1. Dudai Y. 1989. The Neurobiology of Memory. Oxford University Press, New York.

Authors
Kaltschmidt, B., & Kaltschmidt, C.
Affiliations
Bielefeld University (DE)
Corresponding author
Kaltschmidt, B.
Venue
Cold Spring Harbor Perspectives in Biology
Published
2009-09-01
Volume
1
Issue
3
Pages
a001271-a001271
ISSN
1943-0264 (ISSN-L)
OpenAlex
W2128916701
Cited by
392
References
78
Citations by year
2026: 15 · 2025: 19 · 2024: 24 · 2023: 15 · 2022: 22 · 2021: 34 · 2020: 34 · 2019: 28 · 2018: 30 · 2017: 29 · 2016: 24 · 2015: 26 · 2014: 26 · 2013: 21 · 2012: 25
Type
posted content
Language
en
Open access
Locations
  • Cold Spring Harbor Perspectives in Biology (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Keywords
NF-κB, nervous system, neuroprotection, learning and memory, glutamatergic neurons, NF-κB p65, P50, retrograde transport, axon growth, glia, neuroinflammation, autoimmune encephalomyelitis, ischemia, Alzheimer's disease
MeSH terms
Animals, Humans, Inflammation, Memory, Mice, Transgenic, Models, Biological, Models, Genetic, Nervous System, Neuroglia, Neurons, Pain, Stem Cells, NF-kappa B, Mice, NF-kappa B p50 Subunit

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