Separating The Therapeutic Benefits Of Cannabis From Its Mood-altering Side-effects

[dyslimbic]

ScienceDaily (Nov. 29, 2007) — Scientists from Queen Mary, University of London, have discovered a new way to separate the therapeutic benefits of cannabis from its mood-altering side-effects.




Cannabis contains a chemical called THC, which binds to, and activates, proteins in the brain known as ‘CB1 cannabinoid receptors’. Activating these receptors can relieve pain and prevent epileptic seizures; but it also causes the mood-altering effect experienced by people who use cannabis as a recreational drug.

Now, Professor Maurice Elphick and Dr Michaela Egertová from Queen Mary’s School of Biological and Chemical Sciences may have found a way of separating out the effects of cannabis – a discovery which could lead to the development of new medicines to treat conditions such as epilepsy, obesity and chronic pain. The research is described in the December issue of the journal Molecular Pharmacology.


http://www.sciencedaily.com/releases/2007/11/071129151109.htm

[soul]

I am sorry but what is wrong with Mood-altering side-effects from MJ, and if indeed does protect our CNS these drug companies are sort of throwing the Wheat out with the Chaff, their not looking at the big picture, you know there is something wrong when they think doing Morphine for MS symptoms is ok
I call it hard core addiction brought to you by your local GP, Neuro, Big Pharma ....
soul

http://www.nature.com/nm/journal/v13/n4/abs/nm1561.html

Journal home > Archive > Letter > Abstract
Letter abstract

Nature Medicine 13, 492 - 497 (2007)
Published online: 1 April 2007 | doi:10.1038/nm1561

Direct suppression of CNS autoimmune inflammation via the cannabinoid receptor CB1 on neurons and CB2 on autoreactive T cells

Katarzyna Maresz1,11, Gareth Pryce2,10,11, Eugene D Ponomarev1, Giovanni Marsicano3, J Ludovic Croxford2,4, Leah P Shriver1,5, Catherine Ledent6, Xiaodong Cheng1, Erica J Carrier7, Monica K Mann1,5, Gavin Giovannoni2,10, Roger G Pertwee8, Takashi Yamamura4, Nancy E Buckley9, Cecilia J Hillard7, Beat Lutz3, David Baker2,10,11 & Bonnie N Dittel1,5,11
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The cannabinoid system is immunomodulatory and has been targeted as a treatment for the central nervous system (CNS) autoimmune disease multiple sclerosis. Using an animal model of multiple sclerosis, experimental autoimmune encephalomyelitis (EAE), we investigated the role of the CB1 and CB2 cannabinoid receptors in regulating CNS autoimmunity. We found that CB1 receptor expression by neurons, but not T cells, was required for cannabinoid-mediated EAE suppression. In contrast, CB2 receptor expression by encephalitogenic T cells was critical for controlling inflammation associated with EAE. CB2-deficient T cells in the CNS during EAE exhibited reduced levels of apoptosis, a higher rate of proliferation and increased production of inflammatory cytokines, resulting in severe clinical disease. Together, our results demonstrate that the cannabinoid system within the CNS plays a critical role in regulating autoimmune inflammation, with the CNS directly suppressing T-cell effector function via the CB2 receptor.
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1. BloodCenter of Wisconsin, Blood Research Institute, Milwaukee, Wisconsin 53226, USA.
2. Department of Neuroinflammation, Institute of Neurology, University College London, London WC1N 1PJ, UK.
3. Department of Physiological Chemistry, Johannes Gutenberg-University Mainz, 55099 Mainz, Germany.
4. Department of Immunology, National Institute of Neuroscience, Tokyo 187-8502, Japan.
5. Department of Microbiology and Molecular Genetics, Medical College of Wisconsin, Milwaukee, Wisconsin 53226, USA.
6. Institut de Recherche Interdisciplinaire en Biologie Humaine et Moleculaire, Université libre de Bruxelles, B-1070 Brussels, Belgium.
7. Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, Wisconsin 53226, USA.
8. Department of Biomedical Sciences, Institute of Medical Sciences, University of Aberdeen, Aberdeen AB25 2ZD, UK.
9. Biological Sciences Department, California State Polytechnic University, Pomona, California 91768, USA.
10. Present address: Neuroimmunology Unit, Neuroscience Centre, Institute of Cell and Molecular Science, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London E1 2AT, UK.
11. These authors contributed equally to this work.