Thin But Persistent Regrowth of Myelin Layers Sign of Health in CNS, Study Says

Iqra Mumal, MSc avatar

by Iqra Mumal, MSc |

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Remyelination

The generation of a thin myelin sheath during remyelination — one that continues to protect nerve cells over time — is indicative of the long-term health and activity of the central nervous system (CNS) in demyelinating diseases such as multiple sclerosis (MS), a new study shows.

These findings, which aim to settle a scientific debate about CNS healing, are reported in the study “Thin myelin sheaths as the hallmark of remyelination persist over time and preserve axon function,” published in the journal PNAS.

The myelin sheath is an insulating layer of lipids (fats) and proteins that wrap around nerves. It works to speed the transmission of signals from the nerves to muscles, in order for a person to carry out activities such as walking, talking, and breathing.

Remyelination, which refers to a process through which the body rebuilds the myelin sheath when it has been stripped away due to disease, is the most powerful form of repair for the brain and the spinal cord in patients with a demyelinating disease. In the recovery phase of a disease, the body will completely remyelinate areas that have been stripped of myelin.

MS is a demyelinating disease, and in these patients remyelination can be quite extensive. The ability of the body to remyelinate nerve cells can also decline as a person ages.

Remyelination is characterized by the presence of thin myelin sheaths. Diameter wise, these new myelin sheaths are thinner than the original myelin layers. While some studies suggest that the myelin layer eventually returns to the original diameter, others suggest that it stay thin.

Researchers at the University of Wisconsin-Madison believe that remyelinated sheaths remain thin, and previously  described observing predominantly thin myelin sheaths in a canine with a demyelinating disorder. But this view remains controversial.

The team, for this reason, conducted a long-term study of two animal models of demyelination.

The first model, studied for more than a decade, was a dog with a genetic developmental delay in myelination. The dogs formed thin myelin sheaths in ways similar to changes seen in remyelinated nerves.

Researchers showed that in this animal model the myelin sheaths remained thin and stable on many axons (nerve cells projections) during the dog’s lifetime, and that these thinner-than-usual myelin sheaths had no detrimental effects on the axons’ ability to transmit nerve impulses or signals.

Next, they studied cats that were undergoing remyelination due to a demyelinating disease. In this animal model, there was significant demyelination of the spinal cord and the optic (eye) nerves. The researchers followed these cats for two years, and demonstrated that the thin myelin sheaths persisted over this period.

“We found that nearly every optic nerve fiber was remyelinated with a thin myelin sheath, which is important for understanding human disease because in multiple sclerosis, the optic nerve is often the first to be demyelinated,” Ian Duncan, the study’s first author, said in a news release.

Overall, researchers demonstrated the importance of remyelination via the production of thin myelin sheaths in the long-term health and function of the CNS. More significantly, they confirmed that the best way of evaluating the health of remyelination and its central nervous system benefits is the persistence of thin myelin sheaths.