Private medical insurance: Scientists like gene flaw to medication failure
Scientists at Oxford University believe they have gotten to the bottom of why a drug which was one considered promising has failed to help people suffering from multiple sclerosis.
Writing in the Nature journal, the researchers said that a genetic variant linked to MS has prevented the drug from taking effect, although it does work for people with other autoimmune diseases.
In fact, they believe that in some cases the drug can make the symptoms of MS worsen, depending on how their genetic make up responds to treatments.
Called anti-TNFs, the medication has been found to be successful for patients suffering from rheumatoid arthritis and inflammatory bowel disease.
The team at Oxford University looked into the mechanics of one particular genetic variant found in a gene called TNFRSF1A and found that it causes the production of an altered and shortened version which "mops up" TND and prevents it from firing signals.
Professor Lars Fugger of the Nuffield Department of Clinical Neurosciences, who led the work, said: "The hope has been that analyses of the whole human genome would lead to findings that are clinically relevant.
"We show that this is possible. It's one of the first such examples, certainly in autoimmune disease."
"Whilst the TNFRSF1A gene variant is linked to a modest risk of developing MS, the drug that mimics the effect of the variant has a considerably greater impact.
"The effects of genetic variants influencing disease risk or resistance can be amplified by drugs. This has often been completely overlooked, but will be critical for using genetic findings in a medical context."
Nick Rijke, director of policy and research at the MS Society, added that there are many genes associated with the condition and little is known about the role they play or how they impact on MS.