The Endocannabinoid System Is Activated during CNS Inflammation and Protects Neurons

[soul]

From all the abstracts and full scientific articles I read, it looks like this substance Medical Marijuana Protects Neurons from Inflammatory Damage

I think this is at least in other countries a very important therapy for MS and other Neurological diseases
I am sure people will disagree with me as, "we need more research" but the current research is so powerful and I have never known a substance that has been researched as much as Marijuana how can an educated MD, Neurologist,Scientist or for that mater the MS patient say this is bunk!


Go searching on the net find out the truth, this stuff can help protect our CNS, by that I mean Medical Grade Cannabis
soul
Summary

Endocannabinoids are released after brain injury and believed to attenuate neuronal damage by binding to CB1 receptors and protecting against excitotoxicity. Such excitotoxic brain lesions initially result in primary destruction of brain parenchyma, which attracts macrophages and microglia. These inflammatory cells release toxic cytokines and free radicals, resulting in secondary neuronal damage. In this study, we show that the endocannabinoid system is highly activated during CNS inflammation and that the endocannabinoid anandamide (AEA) protects neurons from inflammatory damage by CB1/2 receptor-mediated rapid induction of mitogen-activated protein kinase phosphatase-1 (MKP-1) in microglial cells associated with histone H3 phoshorylation of the mkp-1 gene sequence. As a result, AEA-induced rapid MKP-1 expression switches off MAPK signal transduction in microglial cells activated by stimulation of pattern recognition receptors. The release of AEA in injured CNS tissue might therefore represent a new mechanism of neuro-immune communication during CNS injury, which controls and limits immune response after primary CNS damage.

Article Outline

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WSS-4HYMDST-B&_user=10&_coverDate=01%2F05%2F2006&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=1b98a4755a2f463c4d2f41caab2f1e1c#sec2.1

[soul]

CUPID stands for Cannabinoid Use in Progressive Inflammatory brain Disease


http://www.mstrust.org.uk/information/a2z/cupid.jsp

http://www.pms.ac.uk/cnrg/cupid.php
soul

[Aiko]

Thanks, Soul! Have you seen this study from Spain? I added the bold highlight :-) -- Aiko

Mol Cell Neurosci. 2007 Apr;34(4):551-61.

Excitotoxicity in a chronic model of multiple sclerosis: Neuroprotective effects of cannabinoids through CB1 and CB2 receptor activation.

Docagne F, Mu*et*n V, Clemente D, Ali C, Loría F, Correa F, Hernang*mez M, Mestre L, Vivien D, Guaza C.

Grupo de Neuroinmunología - Instituto Ram*n y Cajal, CSIC -Avda Dr Arce, 37 - 28002 Madrid, Spain.

Inflammation, autoimmune response, demyelination and axonal damage are thought to participate in the pathogenesis of multiple sclerosis (MS). Understanding whether axonal damage causes or originates from demyelination is a crucial issue. Excitotoxic processes may be responsible for white matter and axonal damage. Experimental and clinical studies indicate that cannabinoids could prove efficient in the treatment of MS. Using a chronic model of MS in mice, we show here that clinical signs and axonal damage in the spinal cord were reduced by the AMPA antagonist, NBQX. Amelioration of symptomatology by the synthetic cannabinoid HU210 was also accompanied by a reduction of axonal damage in this model. Moreover, HU210 reduced AMPA-induced excitotoxicity both in vivo and in vitro through the obligatory activation of both CB1 and CB2 cannabinoid receptors. Together, these data underline the implication of excitotoxic processes in demyelinating pathologies such as MS and the potential therapeutic properties of cannabinoids.

[soul]

Yes I have that one Aiko there is quite a bit out there and Spain seems to be really helping to make inroads into Cannabinoid Research
If your interested in more Science and research in this area PM me I have quite a bit.
soul
Abstract from Nature medicine 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

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

[soul]

Direct suppression of CNS autoimmune inflammation via the cannabinoid receptor CB(1) on neurons and CB(2) on autoreactive T cells.
[My paper] Katarzyna Maresz , Gareth Pryce , Eugene D Ponomarev , Giovanni Marsicano , J Ludovic Croxford , Leah P Shriver , Catherine Ledent , Xiaodong Cheng , Erica J Carrier , Monica K Mann , Gavin Giovannoni , Roger G Pertwee , Takashi Yamamura , Nancy E Buckley , Cecilia J Hillard , Beat Lutz , David Baker , Bonnie N Dittel

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 CB(1) and CB(2) cannabinoid receptors in regulating CNS autoimmunity. We found that CB(1) receptor expression by neurons, but not T cells, was required for cannabinoid-mediated EAE suppression. In contrast, CB(2) receptor expression by encephalitogenic T cells was critical for controlling inflammation associated with EAE. CB(2)-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 CB(2) receptor.
soul