Multiple sclerosis (MS) is characterized by autoimmune damage to the central nervous system. All the current drugs for MS target the immune system. Although effective in reducing new lesions, they have limited effects in preventing the progression of disability. Promoting oligodendrocyte-mediated remyelination and recovery of neurons are the new directions of MS therapy. The endogenous opioid system, consisting of mu, delta and kappa opioid receptors MOR, DOR, KOR and their ligands, has been suggested to participate in the pathogenesis of MS. However, the exact receptor and mechanism remain elusive. Here we show that genetic deletion of KOR exacerbates experimental autoimmune encephalomyelitis, whereas activating KOR with agonists alleviates the symptoms. KOR does not affect immune cell differentiation and function. Instead, it promotes oligodendrocyte differentiation and myelination both in vitro and in vivo. Our study suggests that targeting KOR might be an intriguing way to develop new MS therapies that may complement the existing immunosuppressive approaches.
Low Dose Naltrexone is a opioid receptor antagonist. At typical dosages, LDN significantly blocks activity at mu- and delta-opioid receptors as well as (to a lesser extent) kappa-opioid receptors.
Does it augment MS…doubt it.
This effect was not at the level of the T cell based on T cell transfer experiments, but it is suggested to be due to an effect on remyelination but in the scenario above, you would expect damage to develop before repair can be initiated but the lines immediately split, so I am not sure that the idea is consistent with that piece of data.