This Is MS Multiple Sclerosis Community: Knowledge & Support

A large magnet perhaps.

Results: MS lesions were visualized using FLAIR and correlated with the absence of zinc by XRF. XRF and SWI showed that in the first MS case, there were large iron deposits proximal to the draining vein of the caudate nucleus as well as iron deposits associated with blood vessels throughout the globus pallidus. Less iron was seen in association with lesions than in the basal ganglia. The presence of larger amounts of iron correlated reasonably well between RS-XRF and SWI. In the second case, the basal ganglia appeared normal and acute perivascular iron deposition was absent.

Conclusion: Perivascular iron deposition is seen in some but not all MS cases, giving credence to the use of SWI to assess iron involvement in MS pathology in vivo

Iron has been implicated in multiple sclerosis for many years. It has been observed by MRI and has been seen in vessel wall for small venules. More recent work has shown that there can be iron build up around MS lesions and inside the lesions although not all lesions show an increase in iron content. Further, different parts of the brain associated with the medial venous drainage system also can show increases in iron content that appear to be affiliated with the draining veins. This iron is often not present MS lesions although in some cases it is and appears as either a uniform intensity or as a ring-like structure around the lesion. Iron in the pulvinar thalamus can increase and is seen in roughly 50% of MS cases especially for young people.

It is quite possible these increases in iron are related to the chronic venous insufficiency and may represent iron in one of three forms: oligodendrocyte ferritin after macrophage activity, iron from blood products or iron in the vessel wall or some combination of these. The iron that is measured here may represent hemosiderin which comes from the breakdown of blood not from other sources of iron. There is no evidence at this time that there are stray sources of iron causing this problem, not has that been proposed in this research. Further, it is unknown what role iron plays at this time and the main effect may remain the demyelinating inflammatory aspects of MS with iron representing either an outcome of endothelial damage or hemosiderin or as part of the inflammatory pathway. Iron has been implicated also in Zamboni's research; one explanation is that it come from a breakdown of ferritin because of a genetic problem related to the stability of ferritin. Much remains to be learned and it is possible that iron may serve as a biomarker for MS.

I believe we are going to learn that this hypoxic injury is more related to RRMS, and the iron deposition is more related to progressive disease.

Would secondary progressive be a case of iron deposition finally catching up to us?

This seems a workable theory. It fits my anecdotal evidence point (RR with flairs repeatedly after altitude). Fatigue would also fit with hypoxia rather than with iron deposition and I have fatigue!

Results: MS lesions were visualized using FLAIR and correlated with the absence of zinc by XRF. XRF and SWI showed that in the first MS case, there were large iron deposits proximal to the draining vein of the caudate nucleus as well as iron deposits associated with blood vessels throughout the globus pallidus.

-Zinc deficiency changes your iron metabolism.
i found an in vitro study; will look for more:
http://www.jbc.org/cgi/content/abstract/283/8/5168
Zinc Deficiency-induced Iron Accumulation
snippets:

Zinc Deficiency-induced Iron Accumulation, a Consequence of Alterations in Iron Regulatory Protein-binding Activity, Iron Transporters, and Iron Storage Proteins*
Abstract
One consequence of zinc deficiency is an elevation in cell and tissue iron concentrations. To examine the mechanism(s) underlying this phenomenon, Swiss 3T3 cells were cultured in zinc-deficient (D, 0.5 μm zinc), zinc-supplemented (S, 50 μm zinc), or control (C, 4 μm zinc) media. After 24 h of culture, cells in the D group were characterized by a 50% decrease in intracellular zinc and a 35% increase in intracellular iron relative to cells in the S and C groups. The increase in cellular iron was associated with increased transferrin receptor 1 protein and mRNA levels and increased ferritin light chain expression. The divalent metal transporter 1(+)iron-responsive element isoform mRNA was decreased during zinc deficiency-induced iron accumulation. Examination of zinc-deficient cells revealed increased binding of iron regulatory protein 2 (IRP2) and decreased binding of IRP1 to a consensus iron-responsive element. The increased IRP2-binding activity in zinc-deficient cells coincided with an increased level of IRP2 protein. The accumulation of IRP2 protein was independent of zinc deficiency-induced intracellular nitric oxide production but was attenuated by the addition of the antioxidant N-acetylcysteine or ascorbate to the D medium. These data support the concept that zinc deficiency can result in alterations in iron transporter, storage, and regulatory proteins, which facilitate iron accumulation.

To confirm the presence of iron deposits and the absence of zinc-rich myelin in lesions, iron and zinc were mapped using RS-XRF. Results: MS lesions were visualized using FLAIR and correlated with the absence of zinc by XRF.