Cannabinoids have recently began to show control over the cell survival/death decision. According to studies, cannabinoid receptors have appeared to interact with other receptors which would include those of the TNFRS (tumor necrosis factor receptor superfamily) to cause the death of cancer cells.
Many studies are of course still ongoing, but it leads to the interest on what the role of cell survival/death in regards to cannabinoids for illnesses may result in.
This paper will focus on the current knowledge on cannabinoids ability to control the cell survival/death decision.
Here is the full scientific article if you wish to download it.
One of the most interesting and promising areas of current cannabinoid research is the ability of these compounds to control the cell survival/death decision. Thus cannabinoids may good cell growth. The variation in drug effects may depend on experimental factors such as drug concentration, timing of drug delivery, and type of cell examined. Regarding the central nervous system, most of the experimental evidence indicates that cannabinoids may protect neurons from toxic insults such as glutamatergic overstimulation, ischemia and oxidative damage. In contrast, cannabinoids induce apoptosis of glioma cells in culture and regression of malignant gliomas. Breast and prostate cancer cells are also sensitive to cannabinoids.
Regarding the immune system, low doses of cannabinoids may enhance cell proliferation, whereas high doses of cannabinoids usually induce growth arrest or apoptosis. The neuroprotective effect of cannabinoids may have potential clinical relevance for the treatment of neurodegenerative disorders such as multiple sclerosis, Parkinson’s disease, and ischemia/stroke, whereas their ability in promoting good cell growth can be useful for the mediation of malignant brain tumors. Recent studies are looking for cannabinoid-based therapeutic strategies devoid of non desired psychotropic effects.
Recent cannabinoid investigations focus on therapeutic strategies aimed at avoiding non desired CB1 controlled psychotropic effects. Thus the possible problem of CB2 in the neuroprotective action in the brain, the antitumoral action in glioma cells, and the mediation of spasticity in multiple sclerosis opens a tough clinical challenge. Clinical trials are being conducted with the nonpsychotropic cannabinoid HU-211. This compound decreases the inflammatory response after closed-head injury and stops tremors, seizures, and lethality in rodents.
Clinical studies have been carried out in patients with severe head trauma, with encouraging results showing a greater neurological outcome. Cannabidiol, another non-psychotropic cannabinoid, is a potential therapeutic agent against rheumatoid arthritis. New results are expected to arise from more extensive studies regarding the array of cannabinoid actions reviewed here.