Cause of Multiple Sclerosis & Other Demyelinating Diseases Given New Explanation By Researchers

Researchers in UC Santa Barbara’s Department of Chemical Engineering have published in theProceedings of the National Academy of the Sciences, the results of a new study explaining the cause of demyelinating diseases, such as Multiple Sclerosis (MS). 

The term demyelination (by which these diseases are classified) describes a loss of myelin in the axons’ sheaths, leading to their degeneration. 

The most common of these diseases is multiple sclerosis.  MS affects approximately 400,000 people in the United states alone, with 200 new reported cases each week.

Myelin acts as insulation around nerve cells and is essential for an efficient and effective transference of the electrical signals along axons through the nervous system, maintaining a rapid transfer of impulses. A lipid bi-layer, proteins, and water compose the myelin layer of insulation.

Dong-Woog Lee, researcher in UCSB and the study’s lead author explains “Basically, myelin is this multiple stacking of lipid bi-layers, they need to be compact, and with very little water between the bilayers.”

Aiming for a molecular approach to myelin membrane interactions, the research group studied the ability of these layers to adhere to each other, considering that even the slightest change in the composition of these myelin bi-layers can affect their ability to insulate the axons.

They deposited a lipid bilayer on a mica substrate before immersing them in a buffer solution containing principally myelin basic protein (MBP), a biomolecule commonly found in myelin sheaths whose principal function is to maintain an optimal structure. Thereafter, with each of the two opposing surfaces on the “surface forces apparatus” (a highly sensitive instrument capable of measuring interactions at the molecular level between membranes), they brought the two bilayers close together, allowing them to interact with each other. Later they pulled them apart, being able to measure the strength of the interaction given by the MBP. They performed this experiment with both healthy myelin and with “disease-like” myelin bilayers.

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