This Is MS Multiple Sclerosis Community: Knowledge & Support

a month later I still havent found that animal study from kansas. Anybody?

Here's my guess based on his mention of Williams and that it is a study of iron deposition:

J Neurochem. 2011 Oct 17. doi: 10.1111/j.1471-4159.2011.07536.x. [Epub ahead of print]

Pathogenic implications of iron accumulation in multiple sclerosis.

Williams R, Buchheit CL, Berman NE, Levine SM.
Department of Molecular & Integrative Physiology, University of Kansas Medical Center, Kansas City, KS Rockhurst University, Kansas City, MO Department of Anatomy & Cell Biology, University of Kansas Medical Center, Kansas City, KS.

Abstract
Iron, an essential element used for a multitude of biochemical reactions, abnormally accumulates in the central nervous system of patients with multiple sclerosis (MS). The mechanisms of abnormal iron deposition in MS are not fully understood, nor do we know whether these deposits have adverse consequences, i.e., contribute to pathogenesis. With some exceptions, excess levels of iron are represented concomitantly in multiple deep gray matter structures often with bilateral representation, while in white matter pathological iron deposits are usually located at sites of inflammation that are associated with veins. These distinct spatial patterns suggest disparate mechanisms of iron accumulation between these regions. Iron has been postulated to promote disease activity in MS by various means: 1) iron can amplify the activated state of microglia resulting in the increased production of proinflammatory mediators; 2) excess intracellular iron deposits could promote mitochondria dysfunction; and 3) improperly managed iron could catalyze the production of damaging reactive oxygen species. The pathological consequences of abnormal iron deposits may be dependent on the affected brain region and/or accumulation process. Here we review putative mechanisms of enhanced iron uptake in MS and address the likely roles of iron in the pathogenesis of this disease.

Journal of Neurochemistry © 2011 International Society for Neurochemistry.

Here's the PubMed link.

He also mentions an article he wrote in this regard:

BMC Neurosci. 2011 Jun 23;12:60.

Iron deposition and inflammation in multiple sclerosis. Which one comes first?

Zivadinov R, Weinstock-Guttman B, Pirko I.
Buffalo Neuroimaging Analysis Center, University at Buffalo, Buffalo, NY, USA. rzivadinov@bnac.net

Abstract
Whether iron deposition is an epiphenomenon of the multiple sclerosis (MS) disease process or may play a primary role in triggering inflammation and disease development remains unclear at this time, and should be studied at the early stages of disease pathogenesis. However, it is difficult to study the relationship between iron deposition and inflammation in early MS due to the delay between the onset of symptoms and diagnosis, and the poor availability of tissue specimens. In a recent article published in BMC Neuroscience, Williams et al. investigated the relationship between inflammation and iron deposition using an original animal model labeled as "cerebral experimental autoimmune encephalomyelitis", which develops CNS perivascular iron deposits. However, the relative contribution of iron deposition vs. inflammation in the pathogenesis and progression of MS remains unknown. Further studies should establish the association between inflammation, reduced blood flow, iron deposition, microglia activation and neurodegeneration. Creating a representative animal model that can study independently such relationship will be the key factor in this endeavor.

PMID: 21699686 [PubMed - in process] PMCID: PMC3141571

And a link to this article.

huh well that's pretty bad news who are hoping for ccsvi->ms sounds like they gave an animal eae and it got ccsvi.

As if eae is a valid way of doing science on ms...

Actually, they don't say the EAE mice got CCSVI, just that there was CNS perivascular iron deposition.


They go on to say that:


It may be splitting hairs, but they seem to be saying that they don't know and we should study this further, not that MS ==> CCSVI, I think.

which is probably a precursor to ccsvi.Or even first stage ccsvi.

If he gave these animals encephalomyelitus by jugular vein occlusion,replicating putnam thats the animal model im after.

Anything on the paediatric study that shows Iron build up very early in the chain ?