Commentary
Methylhonokiol attenuates neuroinflammation: a role for cannabinoid receptors?
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
Journal of Neuroinflammation 2012, 9:135 doi:10.1186/1742-2094-9-135
Published: 20 June 2012Abstract
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.
