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Early research into a treatment for progressive MS.
10 October 2007
Scientists in Scotland may be on the way to discovering the cause of long term disability in people with multiple sclerosis (MS).
New research carried out at the University of Aberdeen in Scotland, led by Professor Chris Linington, showed that some people with MS have specific antibodies (a type of immune molecule) which attack nerve fibres.
The newly identified antibodies recognise and attack a protein called neurofascin–186 which makes up part of the nerve fibre. Higher levels of these antibodies were discovered in a small study of people with MS who have a particularly degenerative type of MS.
Researchers are now planning a larger study and if further research showed the antibody to be responsible, it may be possible to remove these antibodies from the blood of people with MS to slow disease progression.
Professor Linington said ‘I am particularly encouraged because there are already treatments available for other antibody mediated conditions. These type of therapies could be very rapidly translated and applied to MS if we confirm our findings’
Millions of nerve fibres are responsible for transmitting messages from our brain to the rest of our body and these nerves are covered in a protective coating called myelin which wraps in bundles around nerve fibres. The gaps which exist between these bundles are very important to allow transmission of nerve impulses along nerve fibres. The neurofascin antibodies can attack the nerve fibres between these gaps in the myelin
In a rat model of MS the attacking antibodies interrupted nerve impulse transmission and worsened disease symptoms by damaging nerve fibres.
Dr Laura Bell, research communications officer at the MS Society, said: ‘Nerve fibre loss is thought to be the primary cause of long term disability in MS though little is known about what causes that loss. This early research provides potential insight into the process and I look forward to seeing the results of the next stage of the study.’
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Scottish Research
