“Δ⁹-tetrahydrocannabinol (Δ⁹-THC) is neuroprotective in models of Parkinson’s disease (PD).
Although CB1 receptors are increased within the basal ganglia of PD patients and animal models, current evidence suggests a role for CB1 receptor-independent mechanisms.
Here, we utilized a human neuronal cell culture PD model to further investigate the protective properties of Δ⁹-THC.
We found CB1 receptor up-regulation in response to MPP+, lactacystin and paraquat and a protective effect of Δ⁹-THC against all three toxins. This neuroprotective effect was not reproduced by the CB1 receptor agonist WIN55,212-2 or blocked by the CB1 antagonist AM251. Furthermore, the antioxidants α-tocopherol and butylhydroxytoluene as well as the antioxidant cannabinoids, nabilone and cannabidiol were unable to elicit the same neuroprotection as Δ⁹-THC.
We have demonstrated up-regulation of the CB1 receptor in direct response to neuronal injury in a human PD cell culture model, and a direct neuronal protective effect of Δ⁹-THC that may be mediated through PPARγ activation.”
https://www.ncbi.nlm.nih.gov/pubmed/22236282
“In conclusion, we have demonstrated up-regulation of the CB1 receptor in a human cell culture model of PD, as well as a direct neuroprotective effect of the phytocannabinoid, Δ9-THC, not mediated by the CB2 receptor. Although a CB1 receptor-mediated effect cannot totally be excluded, we propose that activation of PPARγ leading to antioxidant effects is highly relevant in mediating the neuroprotection afforded by Δ9-THC in our model.”
http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2990.2011.01248.x/full
Thanks for the sensible critique. Me & my neighbor were just preparing to do a little research about this. We got a grab a book from our area library but I think I learned more from this post. I’m very glad to see such wonderful information being shared freely out there.