Readers of this page will know that we've been looking at the vascular connection to MS. It's long been known that pwMS have "fibrinous exudation", or deposits of fibrinogen in the brain around lesions. Here's a paper on this from Adams et al in 1985.
http://www.direct-ms.org/sites/default/files/Adams%20inflammatory%20vasculititis%20MS%2085.pdf
New research is showing how this fibrinogen breaks through the blood brain barrier and initiates inflammation and nerve damage.
To explain the link of fibrinogen and CCSVI, here is a section of note from a year ago, on "What's blood got to do with it?"
Researchers are honing in on fibrinogen as a mediator in vascular disease, and they are also finding a link in MS.
Fibrinogen is a protein which is made in our livers. It's the sigaling protein for fibrin, which allows our blood to clot. When people develop venous ulcers on their legs, due to chronic venous insufficiency, it's fibrinogen that leaks from the veins and creates a build up of fibrin, depleting the tissue of oxygen and allowing those hallmark ulcers to form. This is called a "fibrin cuff." It's fibrinogen which initiates the coagulation cascade and causes our blood to thicken, as a response to low oxygen levels.
Dr. Zamboni was the first to suggest that MS lesions looked alot like venous ulcers because of the fibrin cuffs found in both sites of injury. And researchers have noted that fibin deposition comes FIRST, before demylination.
link to note "What's Blood Got to Do with it?"
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Today, there is new research showing the connection between fibrinogen and inflammation in the brain. And it appears Dr. Zamboni's theory on venous congestion and fibrin cuffs may very well be correct.
http://www.sciencedaily.com/releases/2012/11/121127154215.htm
"Dr. Akassoglou has focused on the role of the blood-brain barrier leak in MS and has discovered that leakage of the blood clotting protein fibrinogen can trigger brain inflammation," said Ursula Utz, Ph.D., M.B.A., a program director at NIH's National Institute of Neurological Disorders and Stroke (NINDS).
Microglia are cells traditionally thought to control immunity in the nervous system. Previous studies suggested that leakage of fibrinogen activates microglia. In this study, Dr. Akassoglou and her colleagues used a cutting-edge imaging technique called two-photon laser scanning microscopy to watch what happens in an animal model of MS.
"Our results provide the first evidence linking leakage of fibrinogen to neuronal damage," said Dr. Akassoglou, "Vascular changes are the instigator of neurotoxicity."
This research was independently sponsored. There was no industry money involved.
In 2006, Dr. Akassoglou received a Presidential Early Career Award for Scientists and Engineers, which honors and supports the finest and most promising researchers early in their careers.
This study was supported by NINDS (NS051470, NS052189, NS066361); the National Cancer Institute (CA082103); the National Center for Research Resources (RR004050), the National Heart, Lung, and Blood Institute (HL096126), the American Heart Association, the Bechtel Foundation, the Dana Program in Brain and Immuno-imaging, the H. Lundbeck A/S, the Howard Hughes Medical Institute, the National Multiple Sclerosis Society, the Nancy Davis Foundation for Multiple Sclerosis, and the March of Dimes.
We need more independent research like this----looking at the blood, the vasculature and the blood brain barrier in MS.
Joan
