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BDNF reverses aging-related microglial activation.

Shih-Ying Wu1, Bo-Syong Pan1, Sheng-Feng Tsai1

  • 1Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan.

Journal of Neuroinflammation
|July 16, 2020
PubMed
Summary

Decreasing brain-derived neurotrophic factor (BDNF) signaling contributes to age-related microglial activation. Upregulating BDNF signaling inhibits this activation through the TrkB-Erk-CREB pathway, offering therapeutic potential for neurodegenerative diseases.

Keywords:
AgingBDNFCREBMicroglial activationNF-кBTrkB

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Area of Science:

  • Neuroscience
  • Immunology
  • Aging Research

Background:

  • Microglial activation is central to age-related neurodegenerative diseases.
  • Brain-derived neurotrophic factor (BDNF) and its receptor TrkB are present in microglia, but their role in age-related microglial activation is understudied.

Purpose of the Study:

  • To investigate the impact of aging on microglial activation and the BDNF-TrkB pathway.
  • To elucidate the mechanisms by which BDNF influences microglial activation and neurotoxicity.

Main Methods:

  • Examined age-related microglial activation and BDNF-TrkB signaling in mice.
  • Utilized pharmacological and genetic methods in microglial cell lines and primary cells.
  • Assessed the effects of BDNF supplementation and TrkB inhibition on microglial activation.

Main Results:

  • Microglial activation increased with age in mice, correlating with decreased BDNF and TrkB levels.
  • BDNF administration reversed age-related microglial activation and reduced LPS-induced activation.
  • BDNF inhibited pro-inflammatory responses in microglia via the TrkB-Erk-CREB pathway, competing with NF-κB activation.

Conclusions:

  • Reduced BDNF-TrkB signaling promotes microglial activation during aging.
  • Enhanced BDNF signaling effectively inhibits microglial activation through the TrkB-Erk-CREB pathway.