Cannabis based drugs inhibit the development of Disease

Ribeiro R, Yu F, Wen J, Vana A, Zhang Y. Therapeutic Potential of a Novel Cannabinoid Agent CB52 in the Mouse Model ofExperimental Autoimmune Encephalomyelitis. Neuroscience. 2013 Sep . doi:pii: S0306-4522(13)00775-6. 10.1016/j.neuroscience.2013.09.005. [Epub ahead of print]
Multiple Sclerosis (MS) is a demyelinating disease which causes inflammation, demyelination, and axonal injury. Currently, there is no cure for the disease. The endocannabinoid system has recently emerged as a promising therapeutic target for MS. The protective mechanisms of cannabinoids are thought to be mediated by activation of cannabinoid receptor 1 (CB1) and 2 (CB2) expressed primarily in neurons and immune cells, respectively. However, the molecular mechanisms and the contribution of each receptor in ameliorating disease progression are still debatable. Although CB1 and CB2 are expressed in oligodendrocytes, the myelin producing cells in the central nervous system, the role of cannabinoids in oligodendrocyte survival has not been well investigated. Using primary cultures of mature oligodendrocytes, we tested the effect of a novel synthetic cannabinoid CB-52 on oligodendrocyte toxicity induced by peroxynitrite, the primary toxic species released by microglia. Interestingly, we found that CB-52 is more potent than a number of broad and selective CB1 and CB2 agonists in protecting oligodendrocytes against peroxynitrite-induced toxicity. (Therefore what else does this molecule bind to?) The protection provided by CB-52 is likely due to its reduction of ERK1/2 phosphorylation and ROS generation in these cells. Using experimental autoimmune encephalomyelitis (EAE), an animal model of MS, we found that CB-52 reduces microglia activation, nitrotyrosine formation, T cell infiltration, oligodendrocyte toxicity, myelin loss and axonal damage in the mouse spinal cord white matter and alleviates the clinical scores when given either before or after disease onset. These effects are reversed by the CB1 receptor antagonist, but not by the CB2 receptor antagonist, suggesting that activation of CB1 receptors contributes significantly to the anti-inflammatory and neuroprotective effects of cannabinoids on MS.

We have shown this already that CB1 can mediate immunoinhibitory effects at high doses and neuroprotective effects at lower doses, but the question is what were the adverse effects? Because in the past only doses that sedated animals were of any value in the immune inhibitory effect. 

Could this be the drug that gets the interest back into neuroprotection

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  • Obviously its anti-inflamatory and neuroprotective. I have MS and have seen good results from taking cannabis based oil (hemp seed oil) in reducing feet swelling, inflammation, and improving MS symptoms overall. If the drug makers can take the addictive THC element out,
    would be great

  • Problem with cannabis is the effects are linked as they are all caused by stimulation of the CB1 receptor located in different parts of the body.

    However there are ways to do this……

  • There would be a lot of people urging that the THC not be taken out- since it makes cannabis actually work! Sativex has THC. Having said that I don't personally endorse, or use or ever have used it – the smell of it makes me sick – undergraduate years at University made it hard to avoid – in the 'good old days' there used to be "smoke ins" on the University Commons. 'Unknown', I have a MS friend who 'indulges' whenever possible I haven't heard him indicate anything other than the joy of being stoned – but your comments and this post will make happy!

    Does Canbex (?) MD's project – have THC in it? Or is that information 'commercial in confidence'?

    • Interesting MD. So it's a treatment that mimics the properties of cannabis to help reduce spasticity associated with MS. Is this correct?

    • That's right. It reduces spasticity associated with MS without having the psychoactive effects of cannabis. This is because it has its effect by activating a potassium channel (BK channel)but does not bind to the cannabis receptor (CB1) that is responsible for the psychoactive effects of cannabis.

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