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The joint meeting of ACTRIMS and ECTRIMS was held in Boston, September 10-13, 2014.   Here are just a few of the highlights from the sessions that I attended.  For much of the meeting, there were three sessions going on at the same time, so I was able to attend only part of the presentations that looked interesting.

As usual, there were many interesting presentations on new treatments.  Stem cells have been an area of interest for the last several years, and the results from early studies in humans are accummulating.  There are a number of issues and concerns regarding the use of stem cells.  If stem cells from a different person are used, one has to be concerned about rejection and stimulating the immune system.  You can use self stem cells, but these are harder to obtain from adults, and may require prolonged growth in culture.  Whether you use self or non-self stem cells, you have to figure out how to get them to the damaged area and how to make them turn into the type of cells that you need there.  In MS, that would be mostly myelin forming cells and other supportive cells.  Whatever the type of stem cell, you have to be concerned that they could form tumors or other undesirable growth.  Dr. Cohen presented results of a 6 month study of 24 patients treated with self stem cells derived from bone marrow.  It took about 2 months to grow the desired number of cells, which were then infused into the blood.  They did not observe any safety concerns. 
Dr. Sadiq reported a similar study with bone marrow derived stem cells at his center, except the cells were injected into the spinal fluid and patients received multiple injections.  They have safety results from 6 patients treated previously, and are starting a larger study.  They have recruited 20 subjects and treated 3.  No safety issues were noted so far.  Although stem cell treatment is attractive, it remains to be proven whether it is safe and effective.  These types of carefully planned studies are the essential first steps, and it will take many years to determine whether stem cells will be a worthwhile treatment for MS.  There has been much work with stem cells done in animal models.  The results suggest that stem cells may improve disease more through effects on the immune system rather than by making new brain cells. 
There were also several reports on more standard treatments.  Daclizumab is a monoclonal antibody that interferes with the IL2 receptor.  A Phase III study comparing over 900 patients treated with daclizumab given by injection every 4 weeks to a similar sized group treated with avonex found a 45% decrease in relapse rate in the daclizumab group compared to the avonex group.   Multiple MRI measures also favored daclizumab. They did not have any serious safety concerns in this study.  This looks like a promising treatment.  There was also a study comparing the effectiveness of a generic glatiramer acetate to copaxone.  Both Copaxone and the interferons are nearing the end of their patents, and I expect that we will see additional efforts at generic medicines, given the incredible expense of the current medicines.  This study used an MRI outcome, and included a placebo group.  The effect of the generic drug on MRI activity was similar to the branded Copaxone.  This study was designed for the European regulatory process, and it remains to be seen whether the FDA will consider it adequate. 

In the scientific portion of the meeting, there were a large number of presentations on the genetics of MS.  There are now over 150 genes identified as contributing to MS risk.  Most of these have a probable function in the immune system, and so support the idea of MS as an autoimmune disease.  Investigators are now combining the genetic data with other types of data to suggest what cell types and metabolic pathways might be involved in MS.  In his talk on the final day, Dr. DeJager noted that many of the implicated genes are also expressed in the brain. 
A second recurring theme in the meeting was the importance of mitochondria for MS.  Mitochondria are the energy generating units of the cell that convert glucose into ATP, a form of energy that the cell can use for multiple essential processes.  Mitochondrial dysfunction seems to be an early event in MS, and loss of mitochondria can cause death of neurons and myelinating cells which have high energy demands compared to other types of cells.  Although the results of mitochondrial dysfunction fit well with the disease course seen in MS, it is not clear what causes the initial damage to the mitochondria. 

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

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