We have written a great deal in other blog posts about the neuroprotective properties of cannabidiol (CBD), and made the general point that there are other cannabinoids that appear to have at least some of these effects as well. This is because, as a group, they are lipophilic, act as anti-inflammatory agents, and cross the blood-brain barrier easily, modulate immune response, and can target many aspects of neurodegeneration. Cannabigerol (CBG), isolated in 1964 but only under close study fairly recently, is one of them. It is non-psychotropic, being a poor CB1 receptor agonist. It is a partial agonist at CB2, a very strong α2‐adrenoceptor agonist, and a moderate 5‐HT1A receptor antagonist. It also interacts with TRP isoforms, including the TRPV1 and 2 channels.
CBG has shown itself to be of beneficial effect in animal models of Huntington's disease, where it acts on gene expression, eases motor symptoms, reduces microglial activation, and, unsurprisingly, attenuates inflammatory response. These effects are likely to be independent of CB1 and CB2, and probably involve activation of PPARγ. In putative therapy, activating microglia could protect neurons through secretion of anti‐inflammatory cytokines like IL‐4 and IL‐10. Avoiding overactivation, which could be damaging, would be of concern, however. It is not known whether CBG could have the same efficacy as the current VMAT inhibitors in use, that decrease levels of monoamines, or even if CBG works independently of that mechanism.
CBG treatment appears to be well tolerated in animal studies, orally and intraperitoneally. Dose formulations and routes of administration have not been determined conclusively for human use. Basic study of safety and efficacy in humans is still needed, as is clarification of mechanism of action.
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The foregoing is a report on trends and developments in the cannabinoid industry. No product described herein is intended to diagnose, treat, cure or prevent any disease or syndrome.
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