Auto-immune Theory Challenged

[NZer1]

Some time ago I found this paper about the Auto-immune Theory being fawled and the initial proof why. Has anyone seen any follow up to this? I found the first article about it on;
http://www.mult-sclerosis.org/news/Mar2004/FaultyImmuneSystemMayNotBeCauseofMS.html
"It is important to bear in mind that this was a study o......f only 12 brains and further work needs to be done to validate the studies findings. However, if this work reflects what is actually happening in multiple sclerosis, then its implications are earth shattering: Multiple sclerosis will no longer be an autoimmune disease. A lot of text books are going to have to be rewritten. Treatments that target inflammation will not not addressing the root cause of the diease. This does not mean that they are not effective to some degree but that they can never be as good as treatments that target the death of the oligodendrocytes. All the animal models of multiple sclerosis are poor representations of the disease in that they are all primarily autoimmune models. Perhaps this is why so many treatments that are so effective in mouse models prove to make no difference to multiple sclerosis in humans. For animal models to be valid, they would need to show the kind of disease process described by Barnett and Prineas. Researchers will need to change direction. Whilst work on oligodendrocyte precursor cells becomes more important than ever, work on describing the inflammation process in multiple sclerosis needs to take a back-seat. Importantly, researchers need to find out why oligodendrocytes are dying and what can be done to stop them

[NZer1]

I have found an answer, MS is not Auto-immune;
Hypoxia, slowed perfusion, white matter lesions and CCSVI
by CCSVI in Multiple Sclerosis on Thursday, December 31, 2009 at 3:06pm
This post is for those who enjoy reading medical research papers and discussing the current diagnostics in MS. If this is not your area, please disregard -

There have been blog comments and internet statements made that this Facebook page is not scientific. While I try to keep the tone of this page less scholarly and open for all to use, I reject the notion that laypeople cannot understand medical research. I believe Dr. Zamboni's research corroborates recent findings regarding hypoxic injury and slowed perfusion in the MS brain.

Several posters refer to their doctors' comments as to the "unique" presentation of MS as an autoimmune disease- oligoclonal banding in CSF, t-cells which are reactive to myelin and white matter lesions on MRI. But these features are not unique to MS. All of these signs are also found as result of hypoxic injuries to the brain: including (but not limited to) stroke, diffuse cerebral hypoxia, dementia and vascular insufficiency- in which the immune system is similarly activated.

MS is a diagnosis of exclusion - diagnosticians can exclude those patients who are old, who have had a stroke, who have been poisoned by carbon monoxide- although these patients may have MRIs that look the same as an MS patient. When the mode of brain injury is apparent, the diagnosis is easier. MS researchers have here-to-fore not had an explanation for injury, and so the autoimmune theory was employed.

Dr. Zamboni is now showing us that there is a mode of brain injury in MS patient- chronic cerebrospinal venous insufficiency created by venous stenosis and reflux, which is directly linked to the slowed perfusion and hypoxic-like lesions found in the MS brain-as well as the degradation of gray matter due to iron deposition.

If, after reading the following papers, you would like to further discuss and debate the validity of this research, I would be happy to engage in civil discussion. If you would rather continue to throw tomatoes from the safety of your blogs - feel free to do so. But know that there is a lot of research that is confirming Dr. Zamboni's findings, and this lay person is reading and comprehending it.
J

Please consider the following research:
Hypoxia-like tissue injury as a component of multiple sclerosis lesions.
Lassmann H.
http://www.ncbi.nlm.nih.gov/pubmed/12559509

Ischemic Demylination:
http://www.ingentaconnect.com/content/maney/nres/2006/00000028/00000003/art00018

Multiple Sclerosis: The Role of MR Imaging
Y. Ge From Department of Radiology/Center for Biomedical Imaging, New York University Medical Center, New York, NY
http://www.ajnr.org/cgi/content/full/27/6/1165

commentary on this research:
Ischemia and Multiple Sclerosis: Perfusion MR Imaging Provides Insight into an Underexplored Pathophysiology
Jack Simon, Guest Editorialista
a University of Colorado Health Sciences Center
http://www.ajnr.org/cgi/content/full/26/6/1306

Deep white matter ischemia
http://rad.usuhs.edu/medpix/parent.php3?mode=single&recnum=1503&table&srchstr&search

Characterizing iron deposition in multiple sclerosis lesions using susceptibility weighted imaging
E. Mark Haacke, PhD,1,3,4 Malek Makki, PhD,1 Yulin Ge, MD,2 Megha Maheshwari, MS,3 Vivek Sehgal, MD,1 Jiani Hu, PhD,1 Madeswaran Selvan, MS,3 Zhen Wu, MD,4 Zahid Latif, RT,1 Yang Xuan, PhD,1 Omar Khan, MD,5 James Garbern, MD, PhD,5 and Robert I. Grossman, MD2
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2650739/

Deep Gray Matter Perfusion in Multiple Sclerosis
Dynamic Susceptibility Contrast Perfusion Magnetic Resonance Imaging at 3 T

Matilde Inglese, MD, PhD; Sun-Jung Park, MS; Glyn Johnson, PhD; James S. Babb, PhD; Laura Miles, PhD; Hina Jaggi, MS; Joseph Herbert, MD; Robert I. Grossman, MD
http://archneur.ama-assn.org/cgi/content/abstract/64/2/196

Changes in cerebral perfusion precede plaque formation in multiple sclerosis: a longitudinal perfusion MRI study
Jens Wuerfel1,3, Judith Bellmann-Strobl1, Peter Brunecker2, Orhan Aktas1, Henry McFarland3, Arno Villringer2 and Frauke Zipp1
1 Institute of Neuroimmunology, Charité, Berlin, 2 Berlin Neuro Imaging Centre, Department of Neurology, Charité, Berlin, Germany and 3 Neuroimmunology Branch, NINDS, NIH, Bethesda, MD, USA
http://brain.oxfordjournals.org/cgi/content/abstract/127/1/111

[NZer1]

Thanks Lu, I think the same. I am really wondering why this either way hasn't been given more air time. It seems to be a part of the puzzle and yet it has been overlooked. I would have thought it would have been given the once over like CCSVI has!

[Lulu54]

Thanks NZer, interesting reading, from what I could understand. LOL

I'm wondering if this paper was from the original research in 2004 and have others studied this as well?

[NZer1]

http://onlinelibrary.wiley.com/doi/10.1002/ana.21800/abstract
Abstract
Objective
CD4 T-cell–dependent macrophage activation directed against a myelin or oligodendrocyte antigen is generally thought to be the mechanism causing myelin destructio...n in multiple sclerosis (MS). However, areas within expanding MS lesions may exhibit prominent oligodendrocyte loss and apoptosis in the absence of infiltrating lymphocytes. The present study was designed to further investigate the inflammatory profile of different regions within rapidly expanding MS lesions.
Methods
Twenty-six active lesions from 11 patients with early MS were serially sectioned and immunostained for T and B cells, plasma cells, ramified microglia, macrophages, monocytes, and CD209-positive dendritic cells. Cell counts were compared in prephagocytic, phagocytic, and immediately postphagocytic areas.
Results
Parenchymal T and B cells were largely absent in areas of initial oligodendrocyte loss and in areas of degenerate and dead myelin infiltrated by myelin phagocytes. In contrast, trailing areas of complete demyelination packed with lipid macrophages, and, in some lesions, regenerating oligodendrocytes, showed large numbers of T cells, B cells, and immunoglobulin G (IgG)-positive plasma cells. Lesions in 2 exceptionally early cases contained relatively few T and B cells, and no IgG-positive plasma cells.
Interpretation
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. Ann Neurol 2009;66:739–753

[NZer1]

I also found this quote from Marc;
http://www.wheelchairkamikaze.com/2010/03/ms-study-blatantly-driven-by-financial.html
It's high time for neurologists and MS researchers to end of their love affair with the autoimmune theory. There is mounting evidence that the immune response that is now thought to be the cause of MS is actually a secondary phenomenon, and that there is an unknown mechanism killing nerve cells well before the immune system gets involved. A recent study (click here for the abstract) by an Australian MS pathologist and his colleagues examined autopsy brain tissue of 15 deceased MS patients, and found that nerve cell death precedes the involvement of the immune system, which appears to be activated by the damage that some unknown entity is doing to brain and spinal cord tissue (click here for an analysis of this study, provided by The Accelerated Cure Project).