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Cannabis Ingredient May Prevent Mad Cow Disease
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
http://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.
http://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.
Press Release: NORML
National Organisation for the Reform of Marijuana Laws (NORML NZ Inc)
PO Box 3307, Auckland
New Zealand
http://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.
http://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.
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My explanation about the cannabidiol and mad cow disease prevention
1. Cannabinoids are antagonists of the NMDA receptors- so neurodegenerative diseases treatment
Excessive activation of glutamate receptors, particularly of the N-methyl-D-aspartate (NMDA) receptor subtype, leads to neuronal degeneration and death.
Since NMDA receptors are one of the most harmful factors in excitotoxicity, antagonists of the receptors have held much promise for the treatment of conditions that involve excitotoxicity, including neurodegenerative diseases. Cannabinoids are known to inhibit calcium channels- glutamate release in schizophrenia and to inhibit progression of certain neurodegenerative diseases (by reducing intracellular calcium release). It was found that glutamate toxicity was reduced by both cannabidiol, a nonpsychoactive constituent of marijuana, and the psychotropic cannabinoid- THC.
2, Cannabinoids are antagonists of the NMDA receptors- so schizophrenia development
Evidence from histological and pharmacological challenge studies indicates that NMDA receptor hypofunction may play an important role in the pathophysiology of schizophrenia. So, marijuana can be a serious problem, because according to the science studies it seems that cannabis use can precipitate schizophrenia in vulnerable individuals (alkoholism, undernutrition…), especially. However, there are other studies about the opposite marijuana effect, so scientists say; „One possibility is that there are good guys and bad guys within cannabis… Maybe the cannabidiol ameliorates some of the effects of the THC and maybe it actually might be good for you if you are psychotic“. I would like to show that there can be a "nutritional theory" (different „body calcium status“ in good and bad guys…) about the cause of schizophrenia based on "calcium deficiency"...
3. The link between the NMDA receptor hyperfunction (neurodegeneration) and hypofunction (schizophrenia)
The goal of my comment is to show that cannabis use can be a proof about this link. See my website http://www.bse-expert.cz , and my opinion- articles in Medical News Today http://www.medicalnewstoday.com/youropinions.php?opinionid=17968 and http://www.medicalnewstoday.com/youropinions.php?opinionid=18538. Because of their central role in neurodegeneration, NMDA receptors have been considered prime therapeutic targets for the development of useful neuroprotective strategies. However, one could imagine that these receptors might be less sensitive to glutamate, and, perhaps, more sensitive to Mg2+ block . So, NMDA receptors may differ in their sensitivity to voltage-dependent Mg2+ block, agonists, and antagonists as a function of their subunit composition.
For more information:
http://www.bse-expert.cz
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