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)http://brain.oxfordjournals.org/cgi/con ... 124/8/1635Histopathological 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.
No lymphocytes, which react to antigens. Just macrophages, which scavenge "foreigners" and clean up rubbish.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.
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 stressorwhen 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
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).sou wrote:Well, alive myelin is not targeted by any MS process.
http://www.ncbi.nlm.nih.gov/pubmed/20035511
No lymphocytes, which react to antigens. Just macrophages, which scavenge "foreigners" and clean up rubbish.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.