Cannabidiol may be effective in preventing bovine spongiforme enzephalopathy (mad cow disease) Scientists at the National Centre for Scientific Research in France, have found that cannabidiol (CBD), a non-psychoactive ingredient in cannabis, may prevent the development of prion diseases, the most well-known being "mad cow disease" or BSE (bovine spongiforme enzephalopathy).
Monday, 17 September 2007, 10:41 am
Press Release: NORML
National Organisation for the Reform of Marijuana Laws (NORML NZ Inc)
PO Box 3307, Auckland
New Zealand
www.norml.org.nz
It is believed that the BSE may be transmitted to humans, where it is known as Creutzfeldt-Jakob disease. The condition is often fatal and spreads easily.
"The latest study adds to the huge amount of scientific evidence supporting the medicinal use of cannabis," said NORML spokesperson Chris Fowlie.
"Green MP Metiria Turei's bill to allow the medicinal use of cannabis should be supported by any MP with a clear head. Unfortunately most politicians act like mad cows whenever cannabis is mentioned."
The infectious agent in prion diseases is believed to be a specific type of misfolded protein called prion. Misfolded prion proteins carry the disease between individuals and cause deterioration of the brain.
The French researchers, who noted that CBD may be a promising agent for the treatment of prion diseases, reported that the non-psychoactive cannabis constituent CBD inhibited the accumulation of prion proteins in both mouse and sheep prion-infected cells, whereas other cannabinoids were either weak or not effective.
Moreover, after infection with mouse scrapie, a prion disease, CBD limited accumulation of the prion protein in the brain and significantly increased the survival time of infected mice. CBD inhibited the nerve damaging effects of prions in a concentration-dependent manner.
www.scoop.co.nz/stories/SC0709/S00040.htm
Source: Dirikoc S, Priola SA, Marella M, Zsuerger N, Chabry J. Nonpsychoactive cannabidiol prevents prion accumulation and protects neurons against prion toxicity. J Neurosci 2007;27(36):9537-44.