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Old 10-01-2006, 01:37 PM #1
Rudemolle Rudemolle is offline
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Default Breakthrough published in Nature

I hate sensationalism/raising (false?) hopes in everybody affected by MS.

But this group of researchers do have some credentials to show. The leader, Prof. Lars Fugger, have received the Descartes Prize (the European "little" Nobel Prize), on the road to this article.

This really is exciting: The two genes responsible for MS is located and their interactions is discribed down to the molecular level!
We are talking the possible ability to fix/regulate or prevent the underlying processes that results in several autoimmune disseases. Not merely modulating immune responses like we do with BetaInteferons.

Way over my head! So:
How about it, XO, being a (silent) fan of yours for several years?.....

And by the way, this is my first post, having been a lurker for too long
I really did miss reading you guys until i found BT2!

http://www.mrc.ac.uk/prn/index/index..._sept_2006.htm

Or

http://www.nature.com/search/execute...&sp_p_1=phrase

Comments?

Regards Simon
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Old 10-01-2006, 02:32 PM #2
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Hi Simon and welcome to BT2.

Thank you for sharing a very interesting article. I don't recall seeing this before. Maybe if we can find a way to fix the genes we will all be healthy again-- wouldnt that be wonderful Or to ramp up the activity from the gene that dampens down the bad acting gene

Ten more years I figure, of waiting for the cure.
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Old 10-01-2006, 08:48 PM #3
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Probably much more than 10 years....nobody knows what the gene product from the ramping down gene is. That is, if there even is a product. Some genes interact at the nucleic acid level---no protein intermediary.

The news of this article is that the unmodulated gene 1 [without the gene 2 present] seems to result in a disease similar to the rare and fatal form of MS.

That the histocompatibility locus is involved in autoimmune diseases has been known for decades. But MS is not a single locus trait, i.e., not simply inherited like brown eyes. There are still more genes to identify.

But interesting article---thanks for posting it.
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Old 10-01-2006, 10:00 PM #4
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Hi Simon, I'm glad that you finally decided to come out of lurking!

I recall The Montel Williams Foundation announcing something similar . . . I don't think it's the same gene (?), but it was published in Nature Genetics in Apr/05.

http://www.montelms.org/NewsEvents#2

Cherie
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Old 10-02-2006, 05:41 AM #5
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Hi Simon,

Thanks for the kind words. A complete understanding of how DR2b limits severity of MS by controlling the immune response should give insight into potential therapeutic strategies to combat the disease. (I'm curious whether this study implies that the genes which lead to autoimmune disease are selectively advantageous, in (e.g.) the way the genes which cause sickle cell anemia provide protection against malaria.)

However the DR2 haploytpe has long been known to confer MS susceptibility, and as Barbara notes the genetics of MS is complex, with multiple genes at work. Not everyone with MS carries DR2 genes.

Identical twin studies have shown the extent to which MS is genetic: if the disease were strictly genetic, 100% of identical twins would get the disease if the other twin got it. But in fact about 25% of twins will develop MS if their (monozygotic) twin sibling develops MS.

(As you may remember, the phase III trial of the new MS drug MBP8298 is only accepting patients with HLA-DR2 or HLA-DR4 genes, which 70 - 80% of MS patients carry.)

Mark
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Old 10-02-2006, 09:00 AM #6
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Thanks for the replys everyone
I'm not the one to argue here. Just being so impressed by the work of Fugger's over the years, and having a gut feeling (!) this and the works of "his" groups is gonna have an impact. At least on the scientific communities around the world. Try google his name...

Well, the ink is hardly dry, and I havenīt read the article (canīt).

Quoting my first link; "Professor Fugger said: 'This is a new way to assess how genes contribute to autoimmune diseases overall.", you are all right in that its not the cause, its about insight in the mechanism involved. Were all getting closer.

Regards Simon
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