The endocannabinoid system is involved in the pathophysiology of Huntington’s Disease (Fernández-Ruiz et al., 2015; Pazos, Sagredo, & Fernández-Ruiz, 2008).
Consistent changes in CB1, PPARα, and NAPE-PLD were observed in a meta-analysis involving patients and animal models of Huntington’s Disease (Laprairie et al., 2015). This suggests the involvement of the endocannabinoid system in Huntington’s Disease.
In mice, motor deficits, synapse loss, and CNS inflammation can be inhibited upon treatment with a CB2 receptor agonist, whereas these effects can be blocked by a CB2 receptor antagonist. These findings confirm that CB2 receptor signaling is associated with Huntington’s Disease (Bouchard et al., 2012).
In a mouse model for Huntington’s (3NP), CBG exhibited neuroprotective activities and ameliorated motor deficits (Valdeolivas et al., 2015).