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In mice, a possible means to counteract MS























When you have multiple sclerosis, your nerves start to leak information. The nerve cells that connect your limbs to your core, and your core to your spine and brain, begin to ferry signals less quickly and accurately. Then they eventually break down themselves. It’s due to a process called “demyelination,” and in mouse models scientists are starting to be able to undo this erosion of the nervous system’s insulating fiber.

Nerves have two non-interchangeable ends: an in-point and an out-point. Signals come in at the big, bulbous cell body, and leave at the fractured ends called dendrites, ferried on to the bulbous body of the next nerve in the sequence. Some nerves, like neurons in the brain, have these two ends fairly close to one another; others, like motor neurons, can be many inches long on their way to the body’s extremities. In either case, the length of the cell, the connection between the in-point and the out-point, is called the axon. It is responsible for carrying signals over whatever distance the signal must travel to get to the next neuron, or its ultimate destination.

As you might imagine, this long portion of the cell is the most important in determining how quickly the cell can fire overall — that is, how quickly the input of information can lead to a corresponding output of information at the far end. When the signal enters the axon, it opens chemical channels on the axon’s surface that let ions flow mostly freely between the interior of the axon and the exterior of the cell — opening the channels at the start of the axon causes ions to flow and change the charge inside the axon. Once this charge has changed enough (a process called “depolarization” as the cell comes into charge equilibrium with the environment), the next set of channels further down the axon is induced to open, which in turn allows enough of a shift in charge to open the next channels, and so on down the entire length of the axon.

Myelin is a fatty substance that wraps the axon to seal it off from the outside world and prevent ion flow whether or not the channels are open. In a myelinated axon, when early channels open and allow ions to flow, these channels “depolarize” the axon all the way down to the next exposed channels. It turns out that this is very useful to signal propagation, and when the signals can “jump” in this way between the bits of axon that are exposed between myelin deposits, the signal-jumping whole can ferry signals much more quickly than an unmodified nerve cell. More to the point, it turns out that a properly formed “myelin sheath” around a neuron is crucial to accurate and reliable signal transmission.

Multiple sclerosis is a disease that affects myelination, causing tremors, inaccurate movements, and even psychiatric problems by robbing nerves of their ability to quickly and accurately ferry a signal on to the next — that is, by robbing nerves of their ability to do the one thing that nerves have to be able to do. And when exposed for long enough, the axons themselves can start to break down, causing even more acute problems.

This team has used a specific cell type isolated from umbilical cord blood (referred to as UCB, or “gross”), called DUOC-01, and injected it into mice that have had their myelin sheathes degraded through toxicity. The cell therapy promoted accelerated re-myelination of axons that had been stripped of the protective coating, and seemed to have the associated behavioral impacts you’d expect.

In a disease like MS, symptoms generally arise from problems with the myelin-creating “oligodendrocyte” cells, so in principle supplementing these diseased cells with working ones should be capable of offsetting the overall problem. MS isn’t born of some myelin-destroying virus or a toxic metabolic product — new myelin created by injected cord blood cells won’t be attacked or broken down, so simply providing a working myelin system could be enough to ease MS symptoms, or treat them entirely.

This study was conducted in mice, as mentioned. But it’s still exciting, because it could lead to an actual treatment for demyelinating diseases — a way for people who already have diseases like MS to improve their health, not just a preventative therapy that asks them to be content with the knowledge that others won’t suffer their fate in the future. The team plans to take their research forward, applying it in more representative demyelinating disease models in the future.

Story Source: The above story is based on materials provided by EXTREMETECH
Note: Materials may be edited for content and length
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