What's blood got to do with it?

Nov. 27, 2012  10:17 AM

NIH researchers find that fibrinogen appears to be "the trigger" which begins neurodegeneration in MS.

http://www.nih.gov/news/health/nov2012/ninds-27.htm

Researchers are honing in on fibrinogen as a mediator in vascular disease, and they are also finding a link in MS.

Fibrinogen is always present in the blood.  The normal range is 200 - 400 milligrams per deciliter (mg/dL).

Fibrinogen is a protein which is made in our livers.  It's the signaling 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 a lot like venous ulcers because of the fibrin cuffs found in both sites of injury.  

 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1633548/

And researchers have noted that fibin deposition comes FIRST, before demyelination.

Here is some recent research on this connection:

Compromised vasculature in the nervous tissue is a pathogenic manifestation apparent in traumatic injuries, such as spinal cord, optic nerve, and sciatic nerve injury, as well as in central nervous system (CNS) diseases with autoimmune characteristics, such as multiple sclerosis (MS) (7). 

Blood-brain barrier (BBB) disruption precedes clinical symptoms in MS patients (8), and fibrin is deposited in the lesions (9, 10), apparently before cerebral tissue injury and demyelination (11). Fibrin deposition also coincides with areas of demyelination (12), as well as with areas of axonal damage.

http://www.pnas.org/content/101/17/6698.full

CCSVI and the blood brain barrier--new research

February 2, 2012 at 8:56am

New research is showing us how the blood brain barrier functions.  Our understanding of what this barrier is and how it works has changed.

We may not see this happening in our neurologists' offices, or in the press, but it is important to understand that independent researchers (those with no connection to pharma) are looking at how CCSVI impacts the blood brain barrier.  I want to share this as encouragement. 

This is from an article written by K.K. Jain, MD on Medlink.  It was originally released in 1998, but Dr. Jain updates this article, as new research emerges.  The last update was in 2011.  

And now it includes CCSVI.  

Professor Jain is a nanotechnology and neurological expert, and serves as associate editor of Medlink Corporations online encyclopedia of neurology.

For over a century it has been recognized that the entry of certain substances into the brain is restricted. The old concept of the blood-brain barrier as a passive, impermeable barrier that segregates blood and brain interstitial fluid is giving way to the idea that the blood-brain barrier is a dynamic conduit for transport between blood and brain of those nutrients, peptides, proteins, or immune cells that have access to certain transport systems localized within the blood-brain barrier membranes.

When the BBB was first described in the 1800s, it was thought to be an impassible wall between blood, cerebrospinal fluid and brain tissue.  But we now understand:

 Key points

  • The blood-brain barrier is an important conduit of nutrients and cells from the blood to the brain.

  • It also has an important function in protecting the brain from the entry of harmful substances.

  • Knowledge of impairment of permeability of the blood-brain barrier in various neurologic disorders is important in understanding the pathomechanisms and devising strategies for management.

  • Permeability of the blood-brain barrier is manipulated for drug delivery to the brain.

Contrast-enhanced MRI in patients with multiple sclerosis show that increased permeability of the blood-brain barrier commonly occurs with this disease. Lymphocyte recruitment into the brain across endothelial cells of the blood-brain barrier, which is otherwise restricted and well regulated, represents a critical event in pathogenesis of multiple sclerosis (Correale and Villa 2007). The changes in capillary permeability often precede T2-weighted MRI evidence of tissue damage. Increased gelatinase B (a type of matrix metalloproteinase) is associated with an open blood-brain barrier on MRI. Steroids may improve capillary function by reducing activity of gelatinase B.

  Various inflammatory factors produced by perivascular cells in multiple sclerosis affect the permeability of the blood-brain barrier. One of these, the intercellular adhesion molecule-1, binds to its leukocyte ligands and allows activated leukocytes entry into the central nervous system. According to 1 hypothesis, pathological reflux of venous flow in the cerebral and spinal veins increases the expression of intercellular adhesion molecule-1 by the cerebrovascular endothelium, which, in turn, could lead to increased permeability of the blood-brain barrier (Simka 2009).

Specialists of the blood brain barrier and cerebral endothelium understand CCSVI.