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Forgive me if this has all ready been discussed.

I saw the Canadian news report & I think the doctor said the reduced blood flow due to CCSVI causes a buildup of iron in the brain.

Is it possible to have the brain tested for iron and has that been done to verify his theory?

Yes- the test is SWI-MRI, and it's being performed right now. Read this thread for information on iron deposition in MS brains-

http://www.thisisms.com/ftopict-8185-ir ... deposition

I went back to reread this thread and have a question about one of Cheer's statements:

cheerleader wrote:\
If we look at the TRUE cause of disability- the only measurement in the brain that correlates to disability is IRON DEPOSITION and HYPOXIC INJURY.

But we do have some studies showing that hypointense lesions (black holes) correspond with disability far more than hyperintense lesions (the white lesions on the MRI). Black holes are evidence of tissue disruption and axonal loss. Thus, black holes are a better prediction of disability. I could go find the article abstracts if anyone would like them.

So I guess my BIG question is: do black holes have more iron in them? Are they part of the "dark areas" that Dr. Haake is talking about?

By the way, I have several black holes and minimal disability so I don't fit with what the studies say linking progression/disability with black holes!

I really hate that phrase "black holes."

Prof8...we agree. Black holes are the same as gray matter injury. Gray matter is the tissue that shows iron deposition on MRI. White matter (myelin) is where the docs have been looking. They count lesions on the white matter, while the real damage is simmering underneath, as iron is deposed in gray matter. Gray matter death causes the black hole or brain atrophy. The brain is an amazing organ and capable of rerouting. Plasticity!
cheer

Thanks Cheer. I'm seeing Dake next week but am just so curious about the SWI testing that looks for iron and damage in the brain b/c of my black holes. Ironically, I am practically anemic with a very low iron store. My ferritin (the protein which stores iron) is 21. Normal is 12 to 160 for women and 18 to 250 for men. I know people have been asking if there is a correlation between blood serum and what's in the brain but I think not.

prof8 wrote:Ironically, I am practically anemic with a very low iron store.

Hi all,

Take a look at marcstck's post "Met with Top Research Honchos Today; Both Open to CCSV" One researcher had an interesting take on iron. There is still so much to debate and learn!

Lora

Cheerleader (Joan) wrote:
Zamboni asserts that the immune system is merely going in to clean up axonal death from iron deposition and hypoxic injury to gray matter...a similar response to what we see in stroke, and also what happens in chronic venous insufficiency in the legs. so...according to Dr. Zamboni's research, we see stenosis comes first, then reflux of blood into the brain (which can be exacerbated by endothelial disruption) which results in what we now call "MS."

Marcstck (Marc) wrote:
Rusty Bromely, the COO of The Myelin Repair Foundation, was open to the notion of CCSVI. Rusty had an interesting take on the matter of iron deposition, saying that he didn't think it was being deposited by the reflux of blood itself. He believed that if CCSVI was indeed responsible for the iron deposition being found in MS brains, it was because the reflux of deoxygenated blood was leading to the death of oligodendrocytes, which in turn were releasing iron into the brain. Needless to say, I was blown away by the fact that he was so well-versed in the theory that he could make that distinction.

Ruthless (Lora) wrote:
I found this information on-line and wanted to share my thoughts.

How does Multiple Sclerosis do it’s Damage? http://www.mult-sclerosis.org/howms.html

The article said “Oligodendrocyes belong to a larger grouping of maintenance cells called glial cells. Their importance has recently become better understood and, as more and more is discovered about MS, the more central oligodendrocytes, or more accurately their death, has become. In some ways, it is fair to say that multiple sclerosis is a disease of oligodendrocytes.”

So if we put the two statements together, Rusty’s & the article mentioned above, we get:

“Oligodendrocyes belong to a larger grouping of maintenance cells called glial cells. Their importance has recently become better understood and, as more and more is discovered about MS, the more central oligodendrocytes, or more accurately their death, has become, because, the reflux of deoxygenated blood in the CCSVI protocol leads to the death of oligodendrocytes, which in turn releases iron into the brain!!!!!!!!!”

I find these thoughts all go together, this is exciting info!! Am I way off base here?

Lora

The plot thickens...

Iron is essential for oligodendrocyte genesis following intraspinal macrophage activation


David L. Schonberga, b and Dana M. McTiguea, b, c, ,

aThe Neuroscience Graduate Studies Program, The Ohio State University, Columbus, OH, USA

bThe Center for Brain and Spinal Cord Repair, The Ohio State University, Columbus, OH, USA

cDepartment of Neuroscience, and The Ohio State University, Columbus, OH, USA


Received 8 October 2008; revised 30 March 2009; accepted 7 April 2009. Available online 15 April 2009.

Abstract
Progenitor proliferation and differentiation are necessary for oligodendrocyte replacement. Previously, we showed that intraspinal activation of microglia and macrophages with the TLR4 agonist lipopolysaccharide (LPS) induced robust oligodendrocyte genesis. In this study we investigated whether this process involves iron since LPS can alter macrophage regulation of iron and its storage protein ferritin, and oligodendrocytes require iron for proper development and myelination. Further, activated macrophages can sequester and release iron and ferritin. We first examined whether iron or ferritin was present following LPS microinjection. Using Perl's stain, we noted a slight increase in iron at 1d, and peak iron levels 3d post-injection coincident with maximal macrophage activation. Ferritin+ cells were prevalent by 3d and included macrophages and NG2 cells (putative oligodendrocyte progenitors). At 7d, ferritin was mainly expressed by new oligodendrocytes prevalent throughout the lesions. Because of the timing and distribution of iron and ferritin after LPS, we next used an iron chelator to test whether free iron was necessary for maximal LPS-induced oligodendrocyte genesis. Chelating iron by Deferasirox (Exjade®) after LPS microinjection significantly reduced the number of proliferating NG2 cells and new oligodendrocytes. Of the remaining oligodendrocytes, there was a 2-fold decrease in those expressing ferritin, revealing that the number of oligodendrocytes with high iron stores was reduced. Collectively, these results establish that iron accumulates after intraspinal TLR4 activation and is required for maximal TLR4-induced oligodendrogenesis. Since TLR4 agonists are abundant in CNS injury/disease sites, these results suggest that iron may be essential for macrophage/oligodendrocyte communication and adult glial replacement.

Keywords: Inflammation; Polydendrocytes; Precursor; Spinal cord injury; Myelin; Toll-like receptor (TLR); Trauma

Call me dumb, but if iron is needed for oligodendrocyte functioning, then by all means it is not a stretch to think that dying oligos will leave iron behind too... I take from this that Iron is good, very good, until it collects in the wrong place with nowhere to go...

Mark

CureIous, good detective work !!

ozarkcanoer wrote:CureIous, good detective work !!

Haha, just another google scientist waiting in the queue...

zap wrote:

prof8 wrote:Ironically, I am practically anemic with a very low iron store.

Oh Zap, I just got this!! Ha ha ha.