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More MS news articles for May 2003

Synthetic Cannabinoid Thwarts Experimental Viral-Induced Chronic-Progressive MS

Apr 24, 2003
By Megan Rauscher
Reuters Health
New York

For the first time, researchers have used a synthetic cannabinoid receptor agonist to effectively treat clinical symptoms of an animal model of primary-progressive multiple sclerosis (MS). Dr. Stephen D. Miller and Dr. J. Ludovic Croxford report their achievement in the April issue of The Journal of Clinical Investigation.

The cannabinoid receptor agonist R(+)WIN55,212 ameliorates progression of clinical disease symptoms in mice with preexisting Theiler murine encephalomyelitis virus-induced demyelinating disease (TMEV-IDD), they report. This mouse model of chronic progressive MS is characterized by Th1-mediated CNS demyelination and spastic hindlimb paralysis.

"Amelioration of clinical disease is associated with downregulation of both virus and myelin epitope-specific Th1 effector functions (delayed-type hypersensitivity and IFN-gamma production)," they report. R(+)WIN55,212 also significantly inhibited levels of the proinflammatory cytokines TNF-alpha, IL1-beta, and IL-6.

"Currently approved therapies for MS including interferon-beta and Copaxone, are effective to some degree in relapsing-remitting MS, but not primary-progressive disease, and both are associated with serious side effects," Dr. Miller told Reuters Health. "We provide evidence that cannabinoid treatment, which lacks serious side effects, also inhibits the differentiation of autoreactive Th1 effector cells."

This study, he added, "provides pre-clinical evidence suggesting that cannabinoids may be promising therapeutic agents for treating autoimmune disorders such as MS, by exerting potent immunoregulatory effects, in addition to providing symptomatic relief of spasticity, neuropathic pain, and bladder dysfunction."

Clinical trials investigating the use of cannabinoids for the symptomatic treatment of MS are underway in the UK and the Netherlands.

J Clin Invest 2003;111:1231-1240.

© 2003 Reuters Ltd