Researchers in UC Santa Barbara’s Department of Chemical Engineering have published in the Proceedings 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 bilayer, 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 bilayers, 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 bilayers 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.
“A lipid bilayer simulating a healthy myelin membrane adsorbs this protein much better than a lipid bilayer simulating a multiple sclerosis-type of myelin membrane,” said Kai Kristiansen, UCSB researcher “the protein attaches more strongly to the lipid bilayer and can make two apposing lipid bilayers adhere more firmly to each other and at a smaller distance.”
A diseased myelin swells with water that seeps in between the double lipid layers, so instead of being a compact film, the MBP layer becomes like a gel. This leads to a decrease in their insulation properties. From there, impulses slow down along the axon, or dissipate before they reach their destinations, causing paralysis and loss of function.
Different from conventional approaches, this study of healthy and diseased myelin bilayers may provide future insights into causes and mechanisms of demyelinating diseases. According to professor Jacob Israelachvili of UCSB, the next step is to develop an instrument that could be used in hospitals and clinics to study the membranes of certain cells, so their domain structure can be an indicator of the progression of a disease. “We are currently planning a collaboration with a local hospital to provide us with such membranes,” he said.