Genetic differences may predict response to beta interferon treatment for people with MS
14 Jan 2008
Researchers have found genetic differences between people who respond to treatment with beta interferon and those who don’t.
There are currently three beta interferon medications which are used to treat relapsing remitting and help to reduce the number and severity of relapses. However, a significant number of people who are treated with beta interferon continue to experience relapses despite treatment. If it was possible to predict who would respond to beta interferon drugs, it would help guide treatment choices early in the course of the condition.
This study represents an important but early step toward finding a way to predict who will do best on certain therapies for MS. It may help determine who and when to treat when adverse effects, inconvenience and the cost of the drug are significant.
Dr Laura Bell, Research Communications Officer for the MS Society said: ‘This early stage study provides some interesting insight into how our genetic makeup can influence people’s responses to beta interferon, as well as helping us understand more about how the drug functions in the body. This type of work may eventually help us progress toward more targeted, personalised treatments in the future, however this of work needs to be confirmed in larger groups of people before any firm conclusions can be drawn.’
The study involved 287 people with relapsing remitting MS who had experienced at least two relapses before beginning treatment with beta interferon. The participants were then monitored for two years while on treatment. Those who had no relapses and no increase in disability (measured by the EDSS scale) over those two years were considered responders. Those who experienced at least two relapses during follow up and an EDSS increase of one point or more were considered non-responders. About half of the people with MS studied were responders, and half were nonresponders.
The screen identified 18 variations in genetic material that were significantly associated with treatment response between responders and nonresponders. These genetic variations also provide some interesting information about how beta interferon drugs may work. For example, two of the variations appear in genes involved in nerve signaling. Some variations were also found to differ between responders and nonresponders in the gene for “glypican-5,” a protein implicated in nerve growth and repair. Other variations existed in the genes for “extracellular matrix proteins,” which may impact how effectively cells involved in the immune response in MS can enter the central nervous system.
This study represents an important but early step toward finding a way to predict who will do best on certain therapies for MS. It may help determine who and when to treat when adverse effects, inconvenience and the cost of the drug are significant.
Dr Laura Bell, Research Communications Officer for the MS Society said: ‘This early stage study provides some interesting insight into how our genetic makeup can influence people’s responses to beta interferon, as well as helping us understand more about how the drug functions in the body. This type of work may eventually help us progress toward more targeted, personalised treatments in the future, however this of work needs to be confirmed in larger groups of people before any firm conclusions can be drawn.’
The study involved 287 people with relapsing remitting MS who had experienced at least two relapses before beginning treatment with beta interferon. The participants were then monitored for two years while on treatment. Those who had no relapses and no increase in disability (measured by the EDSS scale) over those two years were considered responders. Those who experienced at least two relapses during follow up and an EDSS increase of one point or more were considered non-responders. About half of the people with MS studied were responders, and half were nonresponders.
The screen identified 18 variations in genetic material that were significantly associated with treatment response between responders and nonresponders. These genetic variations also provide some interesting information about how beta interferon drugs may work. For example, two of the variations appear in genes involved in nerve signaling. Some variations were also found to differ between responders and nonresponders in the gene for “glypican-5,” a protein implicated in nerve growth and repair. Other variations existed in the genes for “extracellular matrix proteins,” which may impact how effectively cells involved in the immune response in MS can enter the central nervous system.
