Possible Biomarker for Multiple Sclerosis Identified

[Webdog]

Possible Biomarker for Multiple Sclerosis Identified
https://neurosciencenews.com/multiple-sclerosis-biomarker-10380/

Summary: Acrolein, a molecule implicated as a metabolic waste product, could be a potential biomarker for multiple sclerosis, researchers report.

A biomarker for multiple sclerosis that could be an early warning for the disease has shown promise in both human and animal testing.

Researchers at Purdue University and the Indiana University School of Medicine found that acrolein, a molecule previously suspected as a metabolic waste product that accumulates in people with certain neurological disorders such as multiple sclerosis and Parkinson’s disease, could possibly be used to help diagnose MS.

“The levels of this compound in urine and blood is correlated — the MS patients that had the highest level of acrolein in the blood also had the highest level in the urine,” he said.

According to Shi, it is, therefore, possible that a high level of acrolein is indicative of more active MS, though low levels of acrolein do not rule out the possibility of having MS. Further study is needed to vailidate these initial observations.

 

[Hutan]

For those of you wondering 'could this acrolein be relevant to ME', this paper (I'll call it the acrolein review paper, so as it's not confused with the paper in the first post) is interesting:
Acrolein and Human Disease: Untangling the Knotty Exposure Scenarios Accompanying Several Diverse Disorders

The main endogenous acrolein-yielding process in terms of its potential involvement in many pathophysiological processes is likely lipid peroxidation (LPO), an autocatalytic degradative process to which unsaturated lipids within cell membranes and fat storage droplets are prone.37 LPO typically accompanies the induction of oxidative stress and is thus implicated in many health conditions, especially those involving chronic inflammation.38

So acrolein is probably not a biomarker of MS versus other things, but might help monitor disease flares. And, if we have chronic inflammation, perhaps levels of acrolein might be high in us too.

But it seems that measuring it is not so easy. It's a reactive molecule. This might explain why I couldn't find any study of acrolein levels in people with ME with a quick google.

3.2. Markers of the “Internal Dose.” The internal dose of a compound is typically estimated by quantitating the parent compound and its metabolites within biofluids collected from exposed individuals. In the case of acrolein, such efforts are complicated by the strong electrophilicity that facilitates reactions with glutathione or tissue macromolecules. The readiness with which blood proteins sustain acrolein adduction43,44 likely lowers free concentrations within the circulation, which may explain why plasma levels of free acrolein are not widely reported within the scientific literature.

Instead, the acrolein review paper suggests that looking for the metabolites of acrolein might be the best way to go.

Compared to the limitations attending estimation of its “free” levels in blood and tissues, measurements of acrolein metabolites are useful indicators of the “internal dose” in many contexts. .. 3HPMA and CEMA hold considerable promise as urinary biomarkers of “whole body” acrolein exposure in diverse disease settings, with the caveat that existing methods for their determination do not reveal whether any acrolein that is excreted in a given disease state is of endogenous origin, exogenous origin, or a combination of both.

That's as far as I can get right now. It would be interesting to see if there have been any measurements of these metabolites in people with ME. The acrolein review paper notes that cyclophosphamide is a major exogenous source of acrolein, with that causing bladder damage in people given cyclophosphamide -- so it's possible that Fluge and Mella may have thought about this and done some measurements of both acrolein and its metabolites.