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ENCEPHALOMYELITIS/ EAE & Cannabis studies completed 

Symptoms represent an acquired complex and debilitating disorder that is characterised by profound fatigue and cognitive problems which do not improve with bed rest and becomes worse with physical and mental exertion

Encephalomyelitis is a general term for inflammation of the brain and spinal cord, describing a number of disorders:

  • Acute disseminated encephalomyelitis or postinfectious encephalomyelitis, a demyelinating disease of the brain and spinal cord, possibly triggered by viral infection;
  • Encephalomyelitis disseminata, a synonym for multiple sclerosis;
  • Equine encephalomyelitis, a potentially fatal mosquito-borne viral disease that infects horses and humans;
  • Myalgic encephalomyelitis, a syndrome involving inflammation of the central nervous system with symptoms of muscle pain and fatigue; the term has sometimes been used interchangeably with chronic fatigue syndrome, though there is still controversy over the distinction.
  • Experimental autoimmune encephalomyelitis (EAE), an animal model of brain inflammation.

1997 - Study ~ Suppression of experimental autoimmune encephalomyelitis by cannabinoids.

2003 - Study ~ Immunoregulation of a viral model of multiple sclerosis using the synthetic cannabinoid R(+) WIN55,212

2005 - Study ~ Cannabinoid-receptor 1 null mice are susceptible to neurofilament damage and caspase 3 activation.

2006 - Study ~ Experimental autoimmune encephalomyelitis disrupts endocannabinoid-mediated neuroprotection

2007 - Study - CB2 cannabinoid receptors as an emerging target for demyelinating diseases: from neuroimmune interactions to cell replacement strategies

2007 - Study - The endocannabinoid system is dysregulated in multiple sclerosis and in experimental autoimmune encephalomyelitis

2007 - Study ~ Control of Spasticity in a Multiple Sclerosis Model is mediated by CB1, not CB2, Cannabinoid Receptors

2007 - Study ~ A Cannabinoid CB2 receptor agonist attenuates experimental autoimmune encephalomyelitis (EAE) and reduces MOG-specific T cell proliferation

2008 - Study ~ The CB(2) cannabinoid receptor controls myeloid progenitor trafficking: involvement in the pathogenesis of an animal model of multiple sclerosis.

2008 - Study ~ CB2 cannabinoid receptors as an emerging target for demyelinating diseases: from neuroimmune interactions to cell replacement strategies

2008 - Study ~ Cannabinoids in the management of spasticity associated with multiple sclerosis

2009 - Study ~ Modulation of cannabinoid receptor activation as a neuroprotective strategy for EAE and stroke.

2011 - Study ~ Administration of 2-arachidonoylglycerol ameliorates both acute and chronic Experimental Autoimmune Encephalomyelitis

2012 - Study ~ Cannabinoid receptor-2-selective agonists improve recovery in experimental autoimmune encephalomyelitis

2012 - Study ~ Cannabinoids ameliorate disease progression in a model of multiple sclerosis in mice, acting preferentially through CB(1) receptor-mediated anti-inflammatory effects.

2012 - Study ~ Cannabinoid receptor 2 agonists inhibit migration of activated dendritic cells via modulation of MMP-9

   

 

 

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The endocannabinoid system is dysregulated in multiple sclerosis and in experimental autoimmune encephalomyelitis


  • Abbreviations:

    AEA
    anandamide
    2-AG
    2-arachidonoylglycerol
    CB
    cannabinoid
    CSF
    cerebrospinal fluid
    EAE
    experimental autoimmune encephalomyelitis
    ECS
    endocannabinoid system
    EPSC
    excitatory postsynaptic current
    FAAH
    fatty acid amide hydrolase
    HP
    holding potential
    IPSC
    inhibitory postsynaptic current
    MS
    multiple sclerosis
    NAPE-PLD
    N-acyl-phosphatidylethanolamines (NAPE)-hydrolysing phospholipase D
    PPR
    paired pulse ratio

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 CB2 cannabinoid receptors as an emerging target for demyelinating diseases: from neuroimmune interactions to cell replacement strategies

 
Br J Pharmacol. 2008 January; 153(2): 216–225.
Published online 2007 September 24. doi: 10.1038/sj.bjp.0707466.
PMCID: PMC2219542
CB2 cannabinoid receptors as an emerging target for demyelinating diseases: from neuroimmune interactions to cell replacement strategies
Á Arévalo-Martín, D García-Ovejero, O Gómez, A Rubio-Araiz, B Navarro-Galve, C Guaza, E Molina-Holgado, and F Molina-Holgado
 
Laboratory of Neuroinflammation, Unidad de Neurología Experimental, Hospital Nacional de Parapléjicos (SESCAM), 45071 Toledo, Spain-Research Unit associated to the Instituto Cajal (CSIC), Madrid, Spain
 
Neuroimmunology Group, Instituto Cajal (CSIC), Madrid, Spain
 
King's College London, The Wolfson Centre for Age-Related Diseases, London, UK
Received July 2, 2007; Revised August 16, 2007; Accepted August 20, 2007.
Amongst the various demyelinating diseases that affect the central nervous system, those induced by an inflammatory response stand out because of their epidemiological relevance. The best known inflammatory-induced demyelinating disease is multiple sclerosis, but the immune response is a common pathogenic mechanism in many other less common pathologies (e.g., acute disseminated encephalomyelitis and acute necrotizing haemorrhagic encephalomyelitis). In all such cases, modulation of the immune response seems to be a logical therapeutic approach. Cannabinoids are well known immunomodulatory molecules that act through CB1 and CB2 receptors. While activation of CB1 receptors has a psychotropic effect, activation of CB2 receptors alone does not. Therefore, to bypass the ethical problems that could result from the treatment of inflammation with psychotropic molecules, considerable effort is being made to study the potential therapeutic value of activating CB2 receptors. In this review we examine the current knowledge and understanding of the utility of cannabinoids as therapeutic molecules for inflammatory-mediated demyelinating pathologies. Moreover, we discuss how CB2 receptor activation is related to the modulation of immunopathogenic states.
Keywords: endocannabinoid system, neuroinflammation, oligodendrocyte, multiple sclerosis, neural stem cells

Introduction
Demyelination is the loss of the myelin sheath that surrounds axons and it may affect both the central nervous system (CNS) and peripheral nervous system (PNS). Demyelinating pathologies may have a primary genetic aetiology (leukodystrophies) or may be the secondary effect of infections, vascular alterations, toxic insults or inflammatory reactions. Regardless of the cause, the result will be the total or partial loss of function in the demyelinated area, depending on the region of the nervous system affected. In this review we shall focus on the CNS demyelinating diseases in which inflammation plays a role in their pathogenesis, like multiple sclerosis (MS). However, we will also discuss other effects mediated by CB2 that are fundamental in demyelinating diseases, including neuronal and glial protection, the regulation of stem/precursor cells and cell replacement. MS is the most frequent neurological disease in young adults. In addition to myelin loss, there is also neuronal damage in MS that further contributes to the symptomatology (Ferguson et al., 1997; Mews et al., 1998; Trapp et al., 1998, 1999). Even though several hypotheses have been proposed to explain its aetiopathology, this issue remains unresolved. Epidemiological studies suggest that MS occurs in a genetically susceptible population that has been in contact with an environmental factor, most probably a viral infection. This triggers an immune response that, by diverse mechanisms is finally directed towards myelin self-peptides (Kurtzke, 1993; Johnson, 1994; Coraddu et al., 1998; Haines et al., 1998). Accordingly, the CSF of MS patients contains antibodies against myelin basic protein (MBP) and myelin oligodendroglial glycoprotein (MOG; Olsson and Nilsson, 1979; Miller et al., 1983). This autoimmune response against myelin peptides has been reproduced in animal models of MS, such as experimental allergic encephalomyelitis (EAE) and Theiler's murine encephalomyelitis virus-induced demyelinating disease (TMEV-IDD; Rauch et al., 1987; Rodriguez et al., 1988; Fujinami, 1989; Yamada et al., 1990). In both MS- and EAE-, activated lymphocytes are detected that recognize several epitopes of myelin proteins and these self-reactive clones have been reported to be involved in the pathogenesis of EAE and TMEV-IDD (Gerety et al., 1994; Steinman, 1996; Schmidt et al., 1997; Pope et al., 1998; Hellings et al., 2002). The main reason for inflammatory-mediated damage is thought to be the release of reactive oxygen and nitrogen species by immune cells, as well as that of proteases, which directly mediate cell damage (Correa et al., 2005a, 2005b). In addition, immune cells release cytotoxic/cytostatic cytokines, that not only cause damage but that may also enhance the release of more reactive species and glutamate by the cells in the surrounding tissue (the pathogenic mechanisms of demyelinating diseases are summarized in Figure 1). Modulation of the immune response could therefore be an important therapeutic approach to treat demyelinating conditions.
Figure 1
Figure 1
Hypothetic immune-mediated demyelinating disease pathogenesis. Primed CD4+ T lymphocytes migrate to the CNS through blood vessels enriched in adhesion molecules. Once in the CNS, DCs or macrophages/microglia acting as APC present the antigen to (more ...)

Since the late 1970s, it was clear that the psychoactive compounds of Cannabis sativa, such as delta-9-tetrahydrocannabinol (Δ9-THC), modulate the inflammatory response (Zimmerman et al., 1977; Smith et al., 1978). In the following years, numerous studies...read entire study

 

 

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