Promising Research for Secondary Progressive MS

Q:  I have had secondary progressive MS for 10 years now. I try to keep up with the latest research but find most of the information out there is on relapse remitting MS. Can you tell me if there is any promising research being done on the treatment of secondary progressive MS?

A:  We have had effective MS treatments for 20 years but limited evidence that any of these treatments modify the course of secondary progressive MS in a meaningful way. During the 1990's treatments were first tested in relapsing remitting MS to determine efficacy against a placebo by using relapse rates as the outcome measure. This outcome measure for determining efficacy is easy and can detect differences between groups in a very short period of time. However, we quickly learned that effective treatments for relapsing remitting MS, at least in terms of reducing relapse rates, rarely were effective in secondary progressive MS clinical trials. Even when a benefit was observed, the clinical meaningfulness of this benefit was questionable. Gradually, we have learned that an effective treatment for secondary progressive MS may require therapies with more diverse mechanisms of action than current approved  treatments. To achieve this goal  will likely require treatment combinations.

Effective treatments  for Secondary progressive MS  must do the following:

1. Prevent or limit the systemic inflammatory response in MS
2. Control the ongoing innate inflammatory response within the nervous system that may even persist independently in secondary progressive MS
3. Protect neurons and support cells from ongoing oxidative stress and other mechanisms of neurodegeneration
4. Assist in remyelination 
5. Assist in neuronal regeneration
   

Right now we are testing therapies that may effect one or two of these mechanisms and there is a lot of hope for these treatments. Tysabri is the most effective treatment to limit the systemic inflammatory response, and if this also controls ongoing innate inflammatory responses could be effective as part of the management approach. The anti-lingo therapies in development could assist in remyelination and perhaps limit neurogeneration. Tecfidera an other drugs in development could help control ongoing neurodegeneration by modifying oxidative stress responses. Even high dose Vitamin D therapy could have protective effects. You will note that I have not mentioned stem cell therapy; it is simply too early to say what role various forms of stem cell therapy will play in our future management of secondary progressive MS. Stay tuned for future updates. They will hopefully emerge quickly in the coming years.

Dr. Kinkel