If it's on your mind and it has to do with multiple sclerosis in any way, post it here.


Postby Loriyas » Thu Sep 18, 2008 5:39 am

Found this on the Accelerated Cure Project website:

<shortened url>
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Postby MrsGeorge » Thu Sep 18, 2008 6:56 am

I would love for it to be true... it probably has a way to go yet before it is 'out there'. Exciting prospects tho!
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Postby cheerleader » Thu Sep 18, 2008 9:18 am

Bromley posted about lingo over here:

bit more skeptical...

Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
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Postby CureOrBust » Fri Sep 19, 2008 2:28 am

I have hopes for this product, but fear it will take time to reach market. The one thing I do feel is avoided from all the text, is reference to loss of neurons. You cant mylinate something that is no longer there.
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Postby TwistedHelix » Tue Sep 23, 2008 6:32 am

I know what you mean, Cure, but it might not be as bleak as that. Lingo 1 is part of the receptor complex which binds Nogo, and when Nogo binds it activates RhoA. This is a major inhibitor of axonal growth, so it might just be that controlling Lingo 1 will release the brakes on axonal regeneration.
The first line of this quote hints at that:
Axon regeneration in the adult CNS is prevented by inhibitors in myelin. These inhibitors seem to modulate RhoA activity by binding to a receptor complex comprising a ligand-binding subunit (the Nogo-66 receptor NgR1) and a signal transducing subunit (the neurotrophin receptor p75). However, in reconstituted non-neuronal systems, NgR1 and p75 together are unable to activate RhoA, suggesting that additional components of the receptor may exist. Here we describe LINGO-1, a nervous system-specific transmembrane protein that binds NgR1 and p75 and that is an additional functional component of the NgR1/p75 signaling complex. In non-neuronal cells, coexpression of human NgR1, p75 and LINGO-1 conferred responsiveness to oligodendrocyte myelin glycoprotein, as measured by RhoA activation. A dominant-negative human LINGO-1 construct attenuated myelin inhibition in transfected primary neuronal cultures. This effect on neurons was mimicked using an exogenously added human LINGO-1-Fc fusion protein. Together these observations suggest that LINGO-1 has an important role in CNS biology.
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