Background: Cannabinoids have been shown to exert beneficial actions in different animal models of multiple sclerosis (MS). However, the use of cannabinoids compounds in human therapy is greatly limited by their psychoactivity. Thus, new hopes in MS therapy have arisen from the evidence for a cannabinoid receptor, termed CB2, which is devoid of psychoactive effects in animal models.
Objective: This review discusses the different mechanisms by which CB2 activation could induce therapeutic actions in MS.
Methods: Particular focus is given to the potential effects on inflammation/autoimmunity, remyelination and neuroprotection.
Conclusion: This review discusses the importance of glial cells in sustaining these effects, as well as the putative secondary effects that would limit the use of CB2 agonists in the treatment of MS.