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The European Committee for Treatment and Research in MS held their annual meeting from September 9-12.  Here are some of the presentations that I found interesting.   

There were reports on a number of clinical trials, mainly of oral agents which are summarized below.
Fingolimod:  Further results from the TRANSFORMS study were reported.  The initial results were reported at AAN earlier this year.  This was a large study with over 400 patients per arm, and fingolimod was compared to interferon rather than using a placebo control.  The effectiveness looks good with over a 50% reduction in relapse rate.  Safety is a concern, since there were 2 fatal virus infections in the treatment group. 
Oral cladribine, further results from the CLARITY study.  Again, the initial results of this study were reported at the AAN, and it was a large study with over 400 patients in each group, with cladribine compared to placebo.  The relapse rate was reduced 58%, and MRI activity decreased 88%.  No safety concerns were identified, but they remain a concern with a cytotoxic drug like this. 
BG12 or fumarate:  This agent is earlier in the clinical trial process.  It reduced relapse rate by about 30% compared to placebo. 
Laquinimod:  they reported safety results which look promising. 
Teriflunomide:  This is another oral agent with immunomodulatory effects.  This was a phase II study with around 40 patients per arm, and the drug was used as an add-on to interferon.  MRI activity decreased by about 80%. 
Atorvastatin in early MS:  this is a cholesterol lowering drug, which may also be useful in MS.  They didn't enroll as many patients as they planned with only 82 total patients, and there wasn't any obvious benefit. 
Dirucotide:  This is a peptide from myelin basic protein, and it was used in a study with over 500 secondary progressive MS patients.  There was no benefit. 
In summary, there are a number of oral treatments in development, some of which may be more effective than our current standard treatments.  The combination of increased effectiveness and safety is elusive.  The single trial in progressive MS was negative, but it is good to see treatments being tried in progressive disease since the majority of drugs are for relapsing MS. 

I heard several presentations of some fresh ideas.  One of the keynote lectures was given by Dr. Prineas, a pathologist, who has some different ideas on the cause of MS. Most researchers focus on the role of autoimmunity in damaging myelin and oligodendrocytes.  Dr. Prineas suggested that the primary problem in MS is that oligodendrocytes die off first, and then the immune cells come in to clean up the myelin debris.  He thinks the primary problem may be with the astrocytes, one of the cells in the brain that provides support to the other cells.  I'm not sure he has a convincing story yet, but he definitely has interesting ideas and a different approach. 
Dr. Derfuss from Dr. Meinl's group gave an excellent talk on the proteins neurofascin and contactin as possible targets of the autoimmune attack in MS.  These are relatively minor proteins, but they are located at the junction where the myelin binds to the axon.  These proteins were first identified by finding myelin proteins that were recognized by antibodies from MS patients, and they have gone on to do experimental work to demonstrate that immune attack on these proteins can cause demyelination.  We definitely need to think beyond myelin basic protein and proteolipid protein as the targets of immune attack, and I think this is a step in the right direction. 
Epstein-Barr virus continues to be controversial.  Some investigators can find it in the brain, and others cannot.  I think it will be a while before that issue is settled. 

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

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