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The annual meeting of the European Committee for Treatment and Research in Multiple Sclerosis was held October 25 to 28, 2017 in Paris.  There were a number of noteworthy presentations. 


New Treatments:  

In the area of new treatments, there were some encouraging results.  Two medicines similar to fingolimod (Gilenya) are in development and reported results from their clinical trials.  Both of these medicines are more selective, and should have less unwanted side effects than fingolimod.  Ozanimod reported their clinical results from two separate trials in relapsing MS.  In one, the relapse rate relative to interferon was decreased by 42% and in the other the relapse rate decreased by 48%.  These numbers are impressive, since they are compared to interferon which already reduces relapse rate.  This corresponds to about a 60% decrease in relapse rate compared to no treatment, which is comparable to fingolimod, as expected.  Cardiac side effects seem to be reduced, but there were still some people with low heart rate.  A second similar agent, siponimod, is further along in development and recently reported a benefit in secondary progressive MS.  They presented MRI results from that study showing a decrease in atrophy. 

A phase II study of Ibudilast for progressive MS demonstrated a decrease of almost 50% in the amount of brain atrophy over 2 years which suggests that it is slowing down disease.  The next step for this treatment will be to demonstrate an effect on progression of disability. 

One disappointing result was the study of laquinimod.  This agent is interesting since it seemed to have a larger effect on progression of disability and brain atrophy in previous trials.  All of our current agents have a larger effect on relapses than they do on worsening of disability.  The study looked at 2 doses of laquinimod compared to placebo, with the primary outcome being progression of disability.  The higher dose had cardiac side effects and neither dose had an effect on disability.  The drug did decrease brain atrophy on MRI and decreased relapses by 20%.    

New Science:

A frequent topic on the scientific side was anti-MOG antibodies.  Myelin oligodendrocyte glycoprotein is a protein expressed on the outside of myelin, and in experimental models, antibodies against this protein cause demyelination.  Some people have antibodies against MOG, but the anti-MOG syndrome seems to be distinct from MS.  Anti-MOG is more common in children, and usually causes optic neuritis or spinal cord inflammation.  It can also cause brain lesions.  I think this antibody will likely be a marker for a distinct syndrome, much like the anti-aquaporin 4 antibodies which are a current marker of neuromyelitis optica (NMO).  I think that we are in the process of splitting MS into many distinct diseases, with anti-aquaporin NMO and anti-MOG syndromes the first to be separated out.  I expect many more syndromes will be recognized in the future. 

Another recurring theme was that there appears to be a soluble factor in the spinal fluid that causes tissue damage in MS.  This was shown by looking at the growth pattern of the brain in children with early MS, measuring the activation of the resident immune cells in the brain, and looking at the locations of demyelination.  The exact component in the spinal fluid that causes damage has not been identified, but Dr. Lassmann gave an excellent talk on the pathology of MS and argued that it was not immunoglobulin. 

Another study that I found interesting was a report on 49 patients diagnosed with primary progressive MS who had whole genome sequencing.  Several of the patients had mutations in genes known to cause neurologic disability, suggesting that many people with a diagnosis of PPMS may have a genetic problem causing nerve degeneration instead of an autoimmune disease.  

J. William Lindsey, MD
University of Texas Multiple Sclerosis Research Group
Houston, Texas

copyright 2007-2018 John William Lindsey