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

Robert Zivadinov*, Bianca Weinstock-Guttman and Istvan Pirko

BMC Neuroscience 2011, 12:60  doi:10.1186/1471-2202-12-60

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Iron, CCSVI, and Autoimmunity

Sara Kreindler   (2011-09-02 14:14)  University of Manitoba email

The finding that iron deposition may not be causally linked to MS raises an intriguing question: Might CCSVI trigger MS in a way that does not depend on iron deposition? It occurs to me that a possible answer might be found by treating the autoimmune and vascular accounts of MS not as competing theories but as different pieces of the puzzle.

Consider the dominant animal model for MS – experimental allergic encephalomyelitis. This model depends on an intracerebral injection of antibodies, as antibodies generated in the body will not cross an intact blood-brain barrier (BBB). There is evidence that the BBB of MS patients is damaged, but it is not yet known why or at what point this damage occurs. The mechanism of venous reflux proposed by the vascular theory constitutes a plausible mechanism whereby the BBB could be breached and antibodies cross over into the brain. What if the key substance that stenosed veins push into the brain is not iron, but antibodies?

This hypothesis would be consistent with both the body of evidence that MS is autoimmune in nature, and the theory that venous abnormality – which is strongly associated with MS, and does not appear to be caused by it – plays an important role in MS etiology. It would also be congruent with Zamboni et al.'s (2009) findings that the liberation procedure appeared to be most effective for relapsing-remitting MS (which, as it involves recurrent acute inflammation, might imply a repeated influx of antibodies) and least so for secondary-progressive.

Perhaps this integrative hypothesis could prove a fruitful avenue of investigation.

Competing interests



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