MS life conference

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MS life conference

Postby bromley » Tue Jul 18, 2006 10:08 am

Dear all,

The UK MS Society held a conference in April - I posted some of the presentations (powerpoint). Some of the speakers did not have electronic presentations (or did not provide them to the UK MS Society). Two of the key presenters were Professor Compston and Professor Neil Scolding. Someone who attended the conference took notes of the presentations which are both very interesting and I thought worth sharing. Prof Scolding is one of the UK's leading MS experts who is looking into stem cells. Prof Compston heads up the Cambidge outfit which includes Dr Alasdair Coles (one of my neuros) who is overseeing the Campath trial - there's quite a positive outlook (which is good! - I did predict that 2006 could be a good year!).

Hope you find the notes of the presentations of interest.

Ian


MS CONFERENCES MANCHESTER INTERNATIONAL CONFERENCE CENTRE /G-MEX CENTRE FRIDAY 21ST APRIL – SUNDAY 23RD APRIL 2006

FRIDAY 21ST APRIL 2006

Prof Alastair Compston from Cambridge (Addenbrookes Hospital):


His talk was possibly the best I've ever seen at an MS conference. My notes do not do it justice-if you get chance to listen to it via the MS Society or MS International Federation websites, make sure you do.

He said that research is now hinting at 4 types (not stages of MS); though in his opinion they were all one disease.

There is no clear environmental trigger, but the most common theory-and with the most evidence-is the Epstein Barr Virus (Mono/Glandular fever). Something in the virus molecularly mimicking the myelin and making the body attack itself by mistake.

Prof Compston says that he believes that those who get MS are exposed to EBV later in childhood compared to those who don't. Genes: they now know the key Gene is on Chromosome 6. This gene produces proteins and molecules that drive the Immune System

He then goes on to discuss treatments saying that remylenation is key. Doing this they know can and will reverse damage as well as stabilising inflammation etc. He says Inflammation is both good and bad. Good because it brings in molecules to repair, but bad when it attacks tissue. Keeping people in the R/R phase by treating Inflammation is key. Early and aggressive anti-inflammatory therapy is going to be very important and will be seen very soon. The DMDs don't help much in S/P MS because the inflammation is too prolonged; it is destroying tissues etc, and also targeting Immune Response.

He says that Stem Cells are important at the moment, but research is badly needed. Embryonic Stem Cells will be key he says. There are 5 factors re Stem Cells:

1. Control; They haven't got this yet.-controlling where the cells go
2. Scale; they need to take a few cells and manipulate them to become billions of nerve cells. They can, and do, currently do this
3. Delivery. Can they put them into the blood stream and can they be clever enough to know where they go. Deliver them to the right place
4. Safety; Can we stop the cells growing. i.e. so they don't turn into tumours etc
5. Effectiveness; Can we make them really effective

The other side of treatment instead of repair (like Stem Cells), is stopping Inflammation. Looking at Campath 1H as the example; in S/P Ms, the Campath seemingly stops the attacks, but does nothing, or little, to stop progression. However, in R/R it seemingly stops inflammation and has a very significant effect on stopping progression. So, once again, the earlier the better.

Within the next 12 months or so he believes we will see key breakthroughs.

He was addressing us as health-care professionals and said as MS researchers there has never been a better time as there is a lot of exciting things and breakthroughs going on.

Someone else asked about stress. Prof Compston said he did not believe stress triggers MS or effects disease course/progression. But he did acknowledge that stress can flare up MS symptoms and make things difficult for MSers.


SATURDAY 22ND APRIL 2006

Professor Neil Scolding-University Of Bristol: Stem Cells, Myelin Repair & MS


Prof Scolding discussed that in early MS, it is only Oligodendrocytes (the cells that make myelin) that are damaged. It is later in MS, or if you have Progressive MS, that things become more complicated.

He says there are the following reasons to be optimistic in early MS:

Reasons why, as we stand, EMBRYONIC Stem Cells can be negative:

*We can’t guarantee which cell type they will turn into

*There could still be axonal loss

*Inflammation

*Multifocal factors

*How can we measure affect?

Also, there is the big worry over whether the stem cells will continue to grow and turn into Teratomas/Tumours, how these stem cells will form, the biology of them, the possibility of infection, the ethics and the chance that as the stem cells are not from your own body, that your body will reject them

Professor Alastair Compston-Cambridge Addenbrookes Hospital:
Why Me? An Overview Of The Role OF Genetics


MS is not a hereditary disease, like Huntington’s. Nor is it the next stage up in terms of an inherited condition (forget the actual technical term), like Cystic Fibrosis. MS has a generic trait.

One factor is the ‘age’ of the European race. For example, the African Race is 150,000 years old. Europeans are 10,000 years old (descending from only 15 people who were the only survivors of the Ice Age!).

So, some problematic generic traits, for want of a better expression, have been ‘watered down’ over the 150,000 years in Africans. Whereas in Europeans, at only 10,000 years, they have not. Problems still exist genetically on some Chromosomes.

They key Gene they now know to be the gene on chromosome 6. Its exact position is 6P26. This chromosome affects the immune system. The gene on chromosome 20 (that turns on Oligodendrocytes to make new myelin) is also important.

There is a massive genetic study, the biggest done, including Prof Compston and his team, that is about to end next month. This has been of 500,000 genetic traits. The results should be known soon.

Professor Compston suggests, though only an idea, that current thinking is that the Epstein Barr Virus is involved as the environmental trigger for MS. What they believe is that the later in childhood you are exposed to EBV Virus, that’s when you develop MS. So, many people could be genetically susceptible to getting MS, but if they weren’t ‘exposed’ late on, but earlier, they may not develop MS. However, another theory is that if your immune system is weakened earlier on in life, this leads you to be more susceptible to MS (by EBV having an affect where it previously would not?).

What they now think is that the immune system produces antibodies to fight off the EBV, but as myelin looks very similar to the antibodies as the EBV does your body unknowingly starts attacking itself via the myelin.

Prof Compston said that by the end of this year and next there will be “an explosion in new info”. He also suggests this is only a theory and that sunlight (Vitamin D ) may also play its role; if you look at the prevalence of MS it tends to be in areas of lesser sunlight (though I suspect ‘bad’ genes, and at least one other factor like a ‘trigger’ would also be needed to development MS)

He says there is nothing you can do to safeguard your kids against MS, but the risk of them developing it is low.

Measles and the Herpes HH6-V Virus were previously thought to be triggers and very well may still be.

If you have MS, then a close Family member is statistically more likely to develop another similar condition. They are more likely than the MSer to develop something (apart from Thyroid problems which are more common in the MSer than the Family members) like Lupus, R.A. etc. This was said as a lady who has MS and who’s Sister has Lupus asked a question.
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Postby Jaded » Wed Jul 19, 2006 2:04 pm

Ian

Thanks - that's a very positive and informative post. I look forward to some of the output - hopefully soon!!

J.
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Postby bromley » Thu Jul 20, 2006 1:47 am

Jade,

I'm seeing Dr Coles at the end of August so will ask him what breakthroughs are likely in the near future. I think they are getting much closer to identifying the genes involved - which may lead to better targets for drugs e.g. specific molecules. The real breakthrough will be when they identify what kicks it off and what drives it on. Re-myelination, repair etc etc - they must be getting nearer. But like you say - please make it sooner rather than later.

Ian


Prof Compston is well known in the UK - here is a pen-portrait if anyone is interested.

http://www.mssociety.org.uk/research/re ... pston.html
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