How CBG protects neurons, fights inflammation, and opens the door for new and improved ways to help people afflicted with Huntington’s disease

In 2015, researchers published an article in the journal, Neurotherapeutics, that looked at the properties of cannabigerol on mice with two different in vivo models of Huntington’s disease (HD).

In one model, the researchers intoxicated mice with 3-nitroproprionate (3NP). When treated with CBG, the mice showed improvements in motor deficits. Moreover, CBG also seemed to preserve striatal neurons against the toxic effects of 3NP. When 3NP sets in at a toxic level, a typical response is reactive microgliosis and an increase in the production of proinflammatory markers. According to the researchers, Valdeolivas et al., CBG appeared to offset this response.

Toxic levels of 3NP also can reduce the antioxidant response levels present. However, CBG also significantly improved those numbers.

The researchers even looked into some of the genes responsible for HD. They found that CBG partially normalized the expression of those genes in one model of mice with HD. PPARy, BDNF, and IGF-1, all showed a “modest improvement” in their gene expression.

Most importantly, however, Valdeolivas et al. noted that CBG showed “a small, but significant, reduction in the aggregation of mutant huntingtin in the striatal parenchyma in CBG-treated animals.”

In other words, the study found a new pathway for potential phytocannabinoid treatments for HD.