Welcome! This blog contains research & information on lifestyle, nutrition and health for those with MS, as well as continuing information on the understanding of the endothelium and heart-brain connection. This blog is informative only--all medical decisions should be discussed with your own physicians.

The posts are searchable---simply type in your topic of interest in the search box at the top left.

Almost all of MS research is initiated and funded by pharmaceutical companies. This maintains the EAE mouse model and the auto-immune paradigm of MS, and continues the 20 billion dollar a year MS treatment industry. But as we learn more about slowed blood flow, gray matter atrophy, and environmental links to MS progression and disability--all things the current drugs do not address--we're discovering more about how to help those with MS.

To learn how this journey began, read my first post from August, 2009. Be well! Joan

Showing posts with label endothelial dysfunction. Show all posts
Showing posts with label endothelial dysfunction. Show all posts

Tuesday, November 27, 2012

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.

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.  

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.

Tuesday, January 24, 2012


Vascular inflammation in MS

January 24, 2012 at 11:42am

The Buffalo team has recently published a study on Lp-PLA2 levels in the blood of people with MS.

Lp-PLA2 is an enzyme that circulates in the blood and attaches to cholesterol in the blood stream.  It is an important marker of inflammation, just like C reactive protein.

Here's more information on Lp-PLA2

Lp-PLA2 is also an important marker in endothelial dysfunction.  This means that the lining of the blood vessels is breaking down and inflamed.

What the Buffalo researchers found is that this enzyme shows up in the blood of pwMS---and levels are significantly higher than in controls.

Lp-PLA2: Inflammatory Biomarker of Vascular Risk in Multiple Sclerosis.

A member of the A2 phospholipase superfamily, the enzyme lipoprotein-associated phospholipase A2 (Lp-PLA2), is involved in atherogenic processes. Lp-PLA2 mass and activity were measured by the enzyme-linked immunosorbent assay and by a colorimetric method, respectively, and compared among 63 multiple sclerosis (MS) patients and 47 age-matched healthy controls (HCs). Lp-PLA2 plasma levels were significantly higher in MS patients (236.7 ± 10 ng/ml) compared to HCs (197.0 ± 7 ng/ml) (p = 0.003)


Here is a study of plasma levels of Lp-PLA2 in those with coronary disease and normals.  Lp-PLA2 is a marker of endothelial dysfunction. ( Note that pwMS had a 236.7 ng/ml level, and those with coronary arterial disease had a 246.2 ng/ml level.  Normals have around a 200 ng/ml level.)