myelin and ccsvi

sbr487 · Post by **sbr487** » Tue Aug 03, 2010 3:15 am

I believe on of the characteristic feature of MS is demyelination process.
In the light of ccsvi, has anyone explained (Dr. Z, Dr. Schelling ...) why myelin is targeted by the immune system?

costumenastional · Post by **costumenastional** » Tue Aug 03, 2010 3:53 am

I have yet to read something regarding this issue. Hopefully someone will come to the rescue. I was wondering too.
I am not an expert of course but i see your question and i raise you another:
what else is there? i mean, what is the first thing an intruder would meet with, once inside the cns? An educated guess would be that everything in there is covered by myelin sealth.
Hopefully we ll get an answer.

Robnl · Post by **Robnl** » Tue Aug 03, 2010 6:04 am

In Holland, there is research for the role of Alfa Beta Crystallin, a protein. Its seems to be that, after an unknown stressor, abc is attacked by the ai. the ai attacks abc in the myelin forming area, so....kind of colleteral damage...Researchers are trying to resolve the ai attacks by adding abc to th body via the bloodstream, so the ai will get used to abc en doesnt attack it anymore.
(this is really in a very small nutshell

)

I am also curious if and how resolving ccsvi affects the myeline problem. I think the problem still exitst after treatment...

Rob

sbr487 · Post by **sbr487** » Tue Aug 03, 2010 6:20 am

I have read a research paper (I did not bookmark at that time and cant find it now) that indicated that it is cns and just myelin that is the target of MS. In a way, it looks like it is still not clear whether the theory that myelin alone gets affected by MS is confirmed.

Here is an excerpt from a paper:

Histopathological analysis revealed that 48% of the hyperintense areas seen on T2-weighted images represented active lesions, including lesions localized in the normal appearing white matter, without apparent loss of myelin but nevertheless showing a variable degree of oedema, small clusters of microglial cells with enhanced major histocompatibility complex class II antigen, CD45 and CD68 antigen expression and a variable number of perivascular lymphocytes around small blood vessels [designated as (p)reactive lesions]. From the macro-scopically not-visible/not-palpable MRI-detected abnormalities, 58% were (p)reactive lesions and 21% contained active demyelinating lesions. In contrast, visible and/or palpable brain tissue samples mainly contained chronic inactive lesions.

http://brain.oxfordjournals.org/cgi/con ... 124/8/1635

To be frank, I dont know what it means but seems to be implying that myelin loss is not always necessary ...

shye · Post by **shye** » Tue Aug 03, 2010 6:46 am

Yeah, but it seems that lesions themselves are not always necessary, and are certainly no longer a marker of MS activity...

sou · Post by **sou** » Tue Aug 03, 2010 7:52 am

Well, alive myelin is not targeted by any MS process.

http://www.ncbi.nlm.nih.gov/pubmed/20035511

Early loss of oligodendrocytes is a prominent feature in tissue bordering rapidly expanding MS lesions. Macrophage activity is largely an innate scavenging response to the presence of degenerate and dead myelin. Adaptive immune activity involving T and B cells is conspicuous chiefly in recently demyelinated tissue, which may show signs of oligodendrocyte regeneration. The findings suggest that plaque formation has some basis other than destructive cell-mediated immunity directed against a myelin or oligodendrocyte antigen.

No lymphocytes, which react to antigens. Just macrophages, which scavenge "foreigners" and clean up rubbish.

mrhodes40 · Post by **mrhodes40** » Tue Aug 03, 2010 7:59 am

Schelling did talk about it, I think about page 32 of his book or so... link is on the research thread

we also discussed it in about march of 09 at length in the big thread somewhere.

bottom line oligodendrocytes die...when they die myelin dies too and as Sou points out then the scavengers come to clean up the dead cells, including myelin.

when people have a stroke they produce many myelin active t cells---why? to clean up the myelin which died as a result of the trauma. venous insufficiency causes trauma of several types including hypoxia which is known to cause death of oligo's when it occurs in the brain

TMrox · Post by **TMrox** » Tue Aug 03, 2010 8:47 am

I found this video in youtube explaining how the immune system works and why it might attack itself with Walt Disney production like.

Everytime I see mentioned T-cells and B-Cells this video comes to mind... can't stop it

shye · Post by **shye** » Wed Aug 04, 2010 4:38 am

thanks TMrox--

Robnl · Post by **Robnl** » Wed Aug 04, 2010 6:15 am

when people have a stroke they produce many myelin active t cells---why? to clean up the myelin which died as a result of the trauma. venous insufficiency causes trauma of several types including hypoxia which is known to cause death of oligo's when it occurs in the brain

This is what is called the 'unknownn stressor' in the ABC research, and causes immune reaction against ABC and thus destroys the oligos and myelin.. CCSVI can be the unknown stressor

Hopefully a trial will take place next year.....then we know if the theory is right...

Rob[/quote]

1eye · Post by **1eye** » Wed Aug 04, 2010 12:45 pm

sou wrote:Well, alive myelin is not targeted by any MS process.

http://www.ncbi.nlm.nih.gov/pubmed/20035511

Early loss of oligodendrocytes is a prominent feature in tissue bordering rapidly expanding MS lesions. Macrophage activity is largely an innate scavenging response to the presence of degenerate and dead myelin. Adaptive immune activity involving T and B cells is conspicuous chiefly in recently demyelinated tissue, which may show signs of oligodendrocyte regeneration. The findings suggest that plaque formation has some basis other than destructive cell-mediated immunity directed against a myelin or oligodendrocyte antigen.
No lymphocytes, which react to antigens. Just macrophages, which scavenge "foreigners" and clean up rubbish.

I too am interested in this thread but I would like to add another query: my MS seems to come with some fairly serious brain atrophy and cell death. In particular I have seen one of my MRIs that has me much more worried than the fairly standard hyperintense (white) lesions (spots) I had when I was RR. It feature 'black holes' or hypointense (black) spots which are much denser than the hyper-intense (white) spots were. From my diagnosis MRI there was atrophy. I think there is more now. What I'm wondering is if any of the cognoscenti of CCSVI has a logical explanation for this change. It would sure be nice to think after my procedure my brain problems would stop (atrophy and nerve cell death).