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The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
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Related Experiment Video

Updated: Dec 19, 2025

Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1β in Human Monocyte-derived Dendritic Cells
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Enduring Changes in Neuronal Function upon Systemic Inflammation Are NLRP3 Inflammasome Dependent.

Marianna M S Beyer1,2, Niklas Lonnemann1,2, Anita Remus1,2

  • 1Division of Cellular Neurobiology, Zoological Institute, Technische Universität Braunschweig, 38106 Braunschweig, Germany.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|June 6, 2020
PubMed
Summary
This summary is machine-generated.

Systemic immune stimulation can impair brain function and neuronal complexity long-term, especially in aged mice. This age-dependent neuroinflammation is mediated by the NLRP3 inflammasome, and its inhibition rescues cognitive deficits.

Keywords:
APP/PS1LPSNLRP3hippocampusneuroinflammationsepsis

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Area of Science:

  • Neuroscience
  • Immunology
  • Pathology

Background:

  • Neuroinflammation is a key feature of neurodegenerative diseases like Alzheimer's.
  • Acute systemic inflammation can negatively impact brain function, but long-term effects are less understood.
  • Peripheral immune stimulation's persistent consequences on the brain require further investigation.

Purpose of the Study:

  • To investigate the long-term consequences of systemic immune stimulation on brain health.
  • To determine the role of age in vulnerability to systemic immune stimulation.
  • To explore the involvement of the NLRP3 inflammasome in mediating these effects.

Main Methods:

  • Systemic immune stimulation using lipopolysaccharide (LPS) in wild-type and APP/PS1 mice.
  • Assessment of neuronal morphology, long-term potentiation (LTP), and spatial learning.
  • Genetic ablation and pharmacological inhibition of the NLRP3 inflammasome.

Main Results:

  • Peripheral LPS stimulation caused age-dependent decreases in neuronal complexity and impaired LTP and spatial learning in aged mice.
  • Aged APP/PS1 mice showed heightened sensitivity to LPS compared to wild-type mice.
  • NLRP3 inflammasome activation was identified as the mediator, and its inhibition or genetic ablation rescued the observed deficits.

Conclusions:

  • Long-term neuroinflammation and cognitive deficits following systemic immune stimulation are age-dependent.
  • The NLRP3 inflammasome plays a critical role in mediating these persistent effects.
  • Targeting the NLRP3 inflammasome may offer therapeutic potential for age-related neuroinflammation.