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Thought I'd posted this before, but can't see it now...

Main Category: Multiple Sclerosis News
Article Date: 01 Oct 2007 - 4:00 PDT

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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.'

Now that looks really promising. I'm sure that once they've got the progressive stages sorted out that they'll have substantially cracked the whole problem. One wonders why the body produces these antibodies. Molecular mimicry?

Hi GG,
Molecular mimicry and Epitope Spreading have long been favourites of mine, simply because they provide an elegant and convincing way to explain how the immune system can recognise self-tissue as alien.
I want to give the writers of this abstract a big hug because, instead of using the tired old "myelin is like the insulation around an electric cable" analogy, they correctly and succinctly described the Nodes of Ranvier, (the gaps between the myelin segments), and saltatory conduction, (the fact that the electrical impulse leaps between these gaps, which is much faster than simply travelling down the neuron).
It is also at these points that the nerve fibre is naked and exposed to excitotoxic compounds and errant white blood cells,

twisted,

This research was posted earlier and at the time I wondered why the patients with PPMS aren't just given the med as guinea pigs to possibly counter the progression.

Since such a med is already on the market for another disease/diseases maybe it will be available quickly.

gwa

Yes Dom, I posted this story on 28 September. I'm sure you are breaching my copyright or something.

The finding was presented at a conference (I think last year) and one of my neuros thought it was the biggest news of that conference.

These sorts of findings need to be pursued quickly to find out if they are of any real value.

I'm getting confused by all the research findings - NOGO, LINGO, neurofascin, osteopontin!

Ian

You think you're confused – – I can't even tell the difference between your posts and mine! Please don't sue for breach of copyright: Christmas is coming and I need all my gold sovereigns to feed the poor little orphans of the village...

Given my celebrity status, you may be a stalker. I'll give my bodyguard a printout of your picture.

My secretary comes in from Northamptonshire (Thrapston), so I'll ask her to keep a lookout when she travels in.

I prefer the old picture of Dom - less threatening.

Ian

Thrapston is only about 4 miles from where I live… Who, exactly, is stalking whom?

gwa wrote:... at the time I wondered why the patients with PPMS aren't just given the med .... Since such a med is already on the market for another disease/diseases maybe it will be available quickly

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'

I read this as saying that similar "technology" is used in other meds, but a med would need to be specifically created (using the same technology) for MS. Did I read it wrong?

Hello Cure,
That was certainly my interpretation of what he said,