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MS drug failure due to gene flaw

9th July 2012

Researchers at Oxford University say they have identified the reason why certain drugs work for conditions such as rheumatoid arthritis but not for people with multiple sclerosis. 

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The team said a genetic variant associated with the condition meant that anti-TNF drugs could worsen symptoms of MS.

The drugs are used to treat arthritis and inflammatory bowel disease but do not work for people with MS and researchers had not known why this was.

The researchers examined a genetic variant found in the gene TNFRSF1A, which had been linked with the danger of developing the condition.

Normally the protein perches on the outside of cells and is responsible for binding the TNF signalling molecule.

However, the genetic variant turns the protein into a "shortened version which mops up TNF" and stops it working.

Professor Lars Fugger of the Nuffield Department of Clinical Neurosciences, 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."

He added: "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."

 

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