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I attended the ECTRIMS meeting in Copenhagen October 2-5.  This is probably the largest scientific MS meeting each year.  There were over 7,500 people and 1000 poster presentations.  They often had as many as three platform sessions at once, so it was impossible to be present at all the interesting talks. 

In contrast to previous years, there were not many presentations on clinical trials of new treatments for MS.  The major clinical trial report was the phase III study of teriflunomide in clinically isolated syndrome.  Teriflunomide has been approved for relasing MS for the last year.  This study tested it in people who have had their very first symptoms of MS.  The benefit and side effects were similar to that seen in their prevoius two studies of relapsing MS. 
There were a few reports of early studies of interesting treatments.  Biogen has an antibody treatment that is supposed to improve remyelination, and they have completed a safety study.  There is also a treatment aimed at endogenous retroviruses in early studies.  Riluzole, a treatment currently used for motor neuron disease, didn’t have any benefit for progressive MS. 

As usual, there were numerous interesting scientific presentations.  One recurring theme this year was the presence of damage to mitochondria as an early and possibly causal event in MS.  Mitochondria supply the energy the cell needs to function, and prevent damage by oxidation.  The role of iron in MS damage was also a frequent topic. 
Dr. Stephen Hauser from UCSF received the Charcot award, and gave an interesting talk on the role of B cells in MS.  B cells are present in the brain and spinal fluid, and treatments that reduce the number of B cells have a marked effect in relapsing MS.   
One session addressed the role of gut bacteria in MS.  The normal gut has a large variety of bacteria, and these bacteria affect the activity of the immune system.  Studies in mice show that bacteria in the gut can affect autoimmune diseases.  The bacteria change depending on exposure, antibiotic treatment and diet. 
The genetics consortium studying MS has now identified over 100 genetic markers for increased risk of MS, with another large batch in the confirmation process.  These genetic data are being combined with other types of information to suggest that the immune system (white blood cells) are the main cause of MS.  One of the long-standing arguments in MS has been whether disease is caused by autoimmune attack on normal myelin, or abnormal myelin causing autoimmunity. 
My particular interest is the role of Epstein-Barr virus in causing MS.  There were an unusual number of presentations on EBV and other viruses.  Increased antibodies to one EBV protein predict more disease activity, and there are EBV infected cells in the spinal fluid.  Dr. Pender from Australia presented results from treating a progressive MS patient with cells to increase immunity to EBV.  HIV infection may protect against MS, or HIV treatment may help in MS. 

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

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