New Ways To Regenerate The Damaged Myelin Sheath That Protects Our Nerves

Today's post from medicalnewstoday.com (see link below) follows on from yesterday's post, in that it highlights the importance of financing research studies which are (despite the lack of progress on the chemists' shelves) revealing new discoveries that will definitely bear fruit for neuropathy patients in the future. This article discusses the discovery of a new MS treatment which has as its basis, the regeneration of myelin. Now as you may remember, myelin is the vital insulation layer around our nerves that protect them against outside degradation and therefore 'short-circuiting'. When the myelin is destroyed, the nerve is no longer protected, leading to misdirected nerve signals and many of the symptoms neuropathy patients are well aware of. The idea that myelin could be regenerated is therefore an exciting one. It's like having your house re-wired to prevent massive short-circuiting. This article concentrates on multiple sclerosis because that's a disease that directly destroys myelin, probably due to the body's own immune system attacking the nervous system and in particular...myelin. However, you can see the potential this may have for other forms of neuropathy and you can see therefore, what a breakthrough this may be. Having said all that, this is a complex article and is not easy to follow for the layman but you should get a good idea of the theories behind it all and maybe that's all you need to form a picture of how your own form of neuropathy may be improved by regenerated myelin sheaths.

Potential new MS drug could regenerate myelin
Published Thursday 19 July 2018 By Catharine Paddock PhD  Fact checked by Jasmin Collier

New research could lead to treatments for multiple sclerosis that regenerate myelin, the fatty coating that insulates nerve fibers and protects signals between brain cells.

Could there be a new MS drug on the way?

Scientists from the University at Buffalo in New York find that the receptor muscarinic type 3 (M3R) is a "key regulator" of remyelination, which is the process that replenishes lost myelin.

M3R is found on the surface of oligodendrocyte progenitor cells (OPCs), the precursors to the cells that make myelin.

A receptor is a cell-surface protein that triggers certain cell functions when it encounters and binds to a matching unique molecule.

The scientists showed that blocking M3R increased remyelination in mice that had human OPCs transplanted into them.

Senior study author Fraser J. Sim, an associate professor of pharmacology and toxicology, and his colleagues report their findings in a paper now published in The Journal of Neuroscience.
Multiple sclerosis and myelin loss

Multiple sclerosis (MS) is a disease that destroys the myelin sheath that surrounds nerve fibers in the central nervous system, which is made up of the brain, spinal cord, and optic nerve.

Many experts believe that the disease develops because the immune system attacks myelin and the cells that make it as though they were a threat.




MS: New findings may 'prevent future loss of brain cells'


Blocking the unique type of cell death behind the destruction of nerve insulation in MS might be a way to halt the disease.


Read now

As myelin is destroyed, it forms lesions that weaken signals that travel along the nerve fibers, leading to disrupted communication between brain cells. Scientists have learned that the disease also damages the nerve cells themselves.

MS has many symptoms, and they can range from mild to severe and depend on which part of the central nervous system is affected.

Common early symptoms include: problems with vision and pain in the eye; weak and stiff muscles, sometimes with painful spasms; tingling in the limbs, face, and trunk; difficulties with balance; and bladder problems.

As the disease progresses, these symptoms may be accompanied by extreme fatigue, changes in mood and concentration, and difficulties with planning and decision-making.

The symptoms can come and go, or they can persist and worsen. They may also vary from person to person, and they can also change in the same individual over time.

Estimates suggest that there are up to 350,000 people living in the United States who have been diagnosed with MS, with women twice as likely to be affected as men.

Oligodendrocytes and myelination

MS arises not just because the myelin degrades, but also because there is a failure to repair it. This has made scientists wonder if destruction of the cells responsible for remyelination might not be the only factor.

They started to investigate the possibility that the precursors of myelinating cells — the OPCs — were failing to multiply and mature. The result would be a shortage of cells for repairing myelin damage.

Eventually, they discovered that blocking muscarinic receptors was a powerful way to get OPCs to mature and speed up remyelination.

But as the authors note, translating this laboratory success into the clinic has been constrained by "poor understanding" of the muscarinic receptor subtype involved and questions about "species differences between rodents and humans."

In earlier work, the team had reported that solifenacin — a drug that was already approved for treating bladder problems — blocked the receptor and promoted remyelination in animals.

However, in that study it was not clear "which specific receptor the drug worked on," explains Prof. Sim. In order to limit undesirable side effects, it would be better to know precisely which receptor subtype to target.

M3R has role in myelin production

In the latest study, the researchers worked with mouse OPCs, human OPCs, and mice with human OPCs transplanted into them.

They discovered that activating the M3R receptor led to cell signals in OPCs that "act to delay differentiation and remyelination."

Further experiments demonstrated that blocking M3R increased remyelination by human OPCs transplanted into mice.

Prof. Sim explains that their new findings put the field in a better position for carrying out clinical trials of drugs that target M3R in MS patients.

"This work establishes that M3R has a functional role and if blocked, could

https://www.medicalnewstoday.com/articles/322520.php