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Open Access Commentary

Methylhonokiol attenuates neuroinflammation: a role for cannabinoid receptors?

Jürg Gertsch1* and Sharon Anavi-Goffer2

Author Affiliations

1 Institute of Biochemistry and Molecular Medicine, National Centre of Competence in Research NCCR TransCure, University of Bern, Bühlstrasse 28, Bern, CH-3012, Switzerland

2 Departments of Behavioral Sciences and Molecular Biology, Ariel University Centre of Samaria, Ariel, 40700, Israel

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Journal of Neuroinflammation 2012, 9:135  doi:10.1186/1742-2094-9-135

Published: 20 June 2012

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.

Keywords:
Alzheimer’s disease; Cannabinoids; CB2 receptors; Endocannabinoid System; Magnolia grandiflora; Medicinal plant; Methylhonokiol