Methylhonokiol attenuates neuroinflammation: a role for cannabinoid receptors?

Jürg Gertsch* (Corresponding Author), Sharon Anavi-Goffer

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

13 Citations (Scopus)
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Abstract

The cannabinoid type-2 G protein-coupled (CB2) receptor is an emerging therapeutic target for pain management and immune system modulation. In a mouse model of Alzheimer’s disease (AD) the orally administered natural product 4′-O-methylhonokiol (MH) has been shown to prevent amyloidogenesis and progression of AD by inhibiting neuroinflammation. In this commentary we discuss an intriguing link between the recently found CB2 receptor-mediated molecular mechanisms of MH and its anti-inflammatory and protective effects in AD animal models. We argue that the novel cannabimimetic MH may exert its beneficial effects via modulation of CB2 receptors expressed in microglial cells and astrocytes. The recent findings provide further evidence for a potential role of CB2 receptors in the pathophysiology of AD, spurring target validation and drug discovery.
Original languageEnglish
Article number135
Number of pages5
JournalJournal of Neuroinflammation
Volume9
DOIs
Publication statusPublished - 20 Jun 2012

Bibliographical note

Acknowledgements
We thank Stefanie Hofer-Reyes for proofreading the manuscript

Keywords

  • Alzheimer’s disease
  • Cannabinoids
  • CB2 receptors
  • Endocannabinoid System
  • Magnolia grandiflora
  • Medicinal plant
  • Methylhonokiol

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