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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
http://www.c-reactive-protein.com/103.htm

Lp-PLA2 is also an important marker in endothelial dysfunction.

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)

http://www.ncbi.nlm.nih.gov/pubmed/22246459

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.)

Patients (172) with no significant coronary artery disease ( Patients with coronary endothelial dysfunction had significantly higher serum concentrations of Lp-PLA2 than those with normal endothelial function (246.2+/-71.6 versus 209+/-56.7 ng/mL; P=0.001). The odds ratio for coronary endothelial dysfunction in patients with Lp-PLA2 in the highest tertile was 3.3 (95% CI, 1.6 to 6.6).
CONCLUSIONS:
Lp-PLA2 is independently associated with coronary artery endothelial dysfunction and is a strong predictor of endothelial dysfunction in humans.

http://www.ncbi.nlm.nih.gov/pubmed/16239595

blood matters,
cheer

It reminds me of the endothelin-1 findings ( http://www.ncbi.nlm.nih.gov/pubmed/11315981 ).

With this new study, the Lp-PLA2 plasma mass and activity were higher in SP than in RR. Not sure what that might mean.

The Lp-PLA2 has nothing to do with vein inflammation? It is only a vascular marker?

right now, Lp-PLA2 is considered a marker, not a cause of inflammation, Cece.
It's proof that the endothelium is not functioning properly, and has become permeable.
What is interesting is, like you said, this marker is higher in SPMS....although we're told pwSPMS no longer have inflammation. What is really true is there is less immune activation, but if we look at this new biomarker, the inflammation remains. And the current immune modulating drugs do not work in SPMS.

There are new studies trying to block this lipoprotein in mice, in preparation for human drug trials.
It appears that inhibiting Lp-PLA2 decreases inflammation....so, it may be a player as well as a marker.
More research ahead!
http://www.plosone.org/article/info%3Ad ... ne.0023425

cheer

The advances being made in the study of "proteins" is very encouraging. Here's another avenue of research in proteins/Alzheimer's.

Prion Protein TPrP http://www.medicalnewstoday.com/releases/241463.php

In the study, the newly identified toxic form of abnormal prion protein, known as TPrP, caused several forms of neuronal damage ranging from apoptosis (programmed cell death) to autophagy, the self-eating of cellular components, as well as molecular signatures remarkably similar to that observed in the brains of prion-infected animals. The study found the most toxic form of prion protein was a specific structure known as alpha-helical.

New Paths to Explore

In addition to the insights it offers into prion diseases such as "mad cow" and a rare human form Creutzfeldt-Jakob disease, the study opens the possibility that similar neurotoxic proteins might be involved in neurodegenerative disorders such as Alzheimer's and Parkinson diseases.

Lora

I mistyped, I was trying to ask if it was a marker of vein inflammation or of brain inflammation, and maybe it is a marker of both and/or either.

Yes, I would've expected less inflammation and therefore less lp-LPA2 in secondary progressive MS, as compared to RR MS, and instead it's the opposite.

Cece wrote:I mistyped, I was trying to ask if it was a marker of vein inflammation or of brain inflammation, and maybe it is a marker of both and/or either.

Yes, I would've expected less inflammation and therefore less lp-LPA2 in secondary progressive MS, as compared to RR MS, and instead it's the opposite.

It's a serum marker, meaning inflammation throughout the whole body.
The blood test for Lp-PLA2 is now being marketed to docs and patients for heart attack and stroke risk---basically just the arterial side of things. But blood travels thru veins and arteries, and as we've learned around here....inflammation affects both. And if veins are suffering due to disturbed blood flow and inflammation, this marker will show up.
http://www.plactest.com/


Here's how they explain the test for laypeople on the site:

When you have an infection in a cut, the cut becomes inflamed and hurts! Your arteries do not have the same type of pain receptors, and are unlikely to hurt when they are inflamed. The PLAC Test measures an enzyme that increases when your arteries are inflamed. That is why the PLAC Test can help your doctor better understand what is happening in your arteries, and assess your risk for heart attack and stroke.

http://www.plactest.com/pdf/literature/ ... atient.pdf
cheer