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Degradation of NLRP3 by p62-dependent-autophagy improves cognitive function in Alzheimer's disease by maintaining the phagocytic function of microglia.

Dongyuan ZhangYu ZhangJirong PanJingjing CaoXiuping SunXianglei LiLing ZhangChuan Qin
Published in: CNS neuroscience & therapeutics (2023)
P62 recognizes and binds to ubiquitin-modified NLRP3. It plays a vital role in regulating the inflammatory response by participating in ALP-associated NLRP3 protein degradation, which improves cognitive function in AD by reducing the pro-inflammatory status and pyroptosis of microglia, thus maintaining its phagocytic function.
Keyphrases
  • inflammatory response
  • nlrp inflammasome
  • lipopolysaccharide induced
  • lps induced
  • toll like receptor
  • neuropathic pain
  • cell death
  • signaling pathway
  • oxidative stress
  • immune response
  • protein protein