Methylhonokiol attenuates neuroinflammation:  a role for cannabinoid receptors?

Jürg Gertsch; Sharon Anavi-Goffer

doi:10.1186/1742-2094-9-135

Methylhonokiol attenuates neuroinflammation: a role for cannabinoid receptors?

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

^*Corresponding author for this work

Applied Medicine

Research output: Contribution to journal › Article › peer-review

12 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 language	English
Article number	135
Number of pages	5
Journal	Journal of Neuroinflammation
Volume	9
DOIs	https://doi.org/10.1186/1742-2094-9-135
Publication status	Published - 20 Jun 2012

Keywords

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

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10.1186/1742-2094-9-135Licence: CC BY

Gertsch_Anavi-Goffer_JoNI_MethylhonokiolAttenuates_VoR
© 2012 Gertsch and Anavi-Goffer.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Final published version, 384 KBLicence: CC BY

Cite this

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title = "Methylhonokiol attenuates neuroinflammation: a role for cannabinoid receptors?",

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{\textquoteright}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{\textquoteright}s disease, Cannabinoids, CB2 receptors, Endocannabinoid System, Magnolia grandiflora, Medicinal plant, Methylhonokiol",

author = "J{\"u}rg Gertsch and Sharon Anavi-Goffer",

note = "Acknowledgements We thank Stefanie Hofer-Reyes for proofreading the manuscript",

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doi = "10.1186/1742-2094-9-135",

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T1 - Methylhonokiol attenuates neuroinflammation

T2 - a role for cannabinoid receptors?

AU - Gertsch, Jürg

AU - Anavi-Goffer, Sharon

N1 - Acknowledgements We thank Stefanie Hofer-Reyes for proofreading the manuscript

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N2 - 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.

AB - 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.

KW - Alzheimer’s disease

KW - Cannabinoids

KW - CB2 receptors

KW - Endocannabinoid System

KW - Magnolia grandiflora

KW - Medicinal plant

KW - Methylhonokiol

U2 - 10.1186/1742-2094-9-135

DO - 10.1186/1742-2094-9-135

M3 - Article

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VL - 9

JO - Journal of Neuroinflammation

JF - Journal of Neuroinflammation

SN - 1742-2094

M1 - 135

ER -

Methylhonokiol attenuates neuroinflammation: a role for cannabinoid receptors?

Abstract

Keywords

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