Madrid, Spain–(ENEWSPF)–March 1, 2012. The administration of a cannabinoid agonist halts the advancement of multiple sclerosis, according to preclinical data to be published in the journal Neuropharmacology.
Investigators at Complutense University in Madrid assessed the impact of WIN55,512-2, a synthetic cannabinoid agonist, in an animal model of multiple sclerosis (MS). Researchers reported that the treatment moderated disease progression and reduced MS symptom, including spasms and tremors.
“In summary, the treatment of EAE (experimental autoimmune encephalomyelitis) mice with the cannabinoid agonist WIN55,512-2 reduced their neurological disability and the progression of the disease,” authors concluded. “This effect was exerted through the activation of CB(1) receptors, which would exert a positive influence in the reduction of inflammatory events linked to the pathogenesis of this disease.”
In 2008, investigators at the University of California at San Diego reported that inhaled cannabis significantly reduced objective measures of pain intensity and spasticity in patients with MS in a placebo-controlled, randomized clinical trial. Researchers concluded, “[S]moked cannabis was superior to placebo in reducing spasticity and pain in patients with multiple sclerosis and provided some benefit beyond currently prescribed treatment.”
Clinical trial data assessing the use of Sativex, a spray containing organic cannabinoid extracts, in MS patients reports, “[L]ong-term use of (the drug) maintains its effect in those patients who perceive initial benefit.” Sativex is presently available by prescription for the treatment of multiple sclerosis in Canada, Denmark, Germany, New Zealand, Spain, and the United Kingdom.”
According to survey data published in 2004 in the journal Neurology, an estimated one in seven patients with MS reports using cannabis therapeutically to treat symptoms of the disease.
Full text of the study, “Cannabinoids ameliorate disease progression in a model of multiple sclerosis in mice, acting preferentially through CB(1) receptor-mediated anti-inflammatory effects,” will appear in the journal Neuropharmacology.