Is myelin sheath destroyed in multiple sclerosis?

In multiple sclerosis, something causes the immune system to attack the central nervous system. That means your nerves won't be able to send and receive messages the way they should. If myelin isn't properly repaired, nerve fibers become increasingly vulnerable to damage. And over time, they can be lost.

When this happens, the messages can no longer be transmitted and the symptoms become permanent. Myelin can be damaged when the body's immune cells think that myelin is a foreign substance. The body's immune system produces inflammatory substances that damage myelin and ultimately destroy the cells (the oligodendrocytes and Schwann cells) that produce myelin. Where the myelin is attacked determines your symptoms.

The destruction of the myelin sheath is called demyelination.

Probably the most well-known disease that attacks the myelin of the central nervous system (brain and spinal cord) is multiple sclerosis.

. Demyelinating disease is any condition that damages the protective covering (myelin sheath) that surrounds nerve fibers in the brain, the nerves that go to the eyes (optic nerves), and the spinal cord. When the myelin sheath is damaged, nerve impulses slow down or even stop, causing neurological problems.

Multiple sclerosis (MS) is the most common demyelinating disease of the central nervous system. In this disorder, the immune system attacks the myelin sheath, or the cells that produce and maintain it. Multiple sclerosis is caused by damage to the myelin sheath. This cover is the protective cover that surrounds nerve cells.

When this nerve covering is damaged, nerve signals slow down or stop. If the sheath is able to repair and regenerate on its own, normal nerve function can return to working properly. However, if the sheath is severely damaged, the underlying nerve fiber can die. The nerve fibers of the central nervous system (brain and spinal cord) cannot fully regenerate on their own.

Therefore, these nerve cells are permanently damaged. Myelin is lost in multiple areas, leaving scar tissue that, due to its hardened characteristics, is called sclerosis. These damaged areas where the sheath has been destroyed and further alter the ability of nerves to transmit messages are also called plaques. These plaques can be identified using magnetic resonance imaging (MRI), a technique that helps doctors evaluate and monitor the progression of multiple sclerosis.

Studies using in vivo demyelination and remyelination models, as well as in vitro culture systems, have revealed a great deal of knowledge about the numerous sequential and necessary steps involved in OPCs to remyelinize a denuded axon. Another factor is that repeated demyelinating attacks, as seen in the form of relapsing and remitting multiple sclerosis, can exhaust the source of OPC, so that remyelination failure can be defined regionally due to the exhaustion of different groups of parents. This is particularly true for the interactions of oligodendroglial cell-derived integrin with axon-derived laminin that contribute to myelination. On the other hand, oligodendrocytes deficient in α1 integrin are unable to wrap around axons, highlighting the role of α1 integrins in promoting the early stages of myelination.

When the myelin sheath is damaged (called demyelination), nerves don't conduct electrical impulses normally. These represent transient contacts between oligodendrocytes and axons that occur during the internodal remodeling process of myelin repair or aberrant interactions. There are several types of advanced magnetic resonance techniques and analytical strategies that can be used to assess damage to the myelin sheath. Another possible function of Cx32 in the SNP is the formation of interstitial junctions between myelinated axons and Schwann cells.

Given the opposing functions observed for the canonical and non-canonical bidirectional function of Notch signaling, it remains to be clarified how this important pathway can be modulated or supported to fully improve remyelination. GM1 is only a minor component of this membrane, while GM4, which is one of the most abundant gangliosides in brain myelin of some species, is absent in the myelin of peripheral nerves. This inflammation leads to demyelination, deterioration and loss of the myelin sheath, and causes axon damage. These complex FMCs with pentacetylation and hexacetylation of all available GalCer hydroxyls are unique and highly hydrophobic myelin lipids with the potential to increase hydrophobic bonds, strengthen myelin membrane lipid interactions, and provoke immune reactions.

Beyond the recruitment and maturation of oligodendrocytes, myelination also requires contact between axons and oligodendrocytes and the creation of multiple envelopes of oligodendrocyte processes around the axon, culminating in the myelin sheath. The best-characterized function of the myelin sheath is to help neurons send electrical signals faster. The MS Society Cambridge Myelin Repair Center is dedicated to understanding more about the myelin repair process, focusing especially on the OPC response. .

Sarah G
Sarah G

Meet Sarah, the driving force behind With a heart for helping others, she's dedicated to providing clear and compassionate guidance to those facing multiple sclerosis. Having witnessed the challenges of MS firsthand, Sarah is committed to empowering individuals with knowledge about early signs, testing, and the resources available.As a trusted source of information, she ensures that offers expert insights and up-to-date content. Sarah's mission is to ease the journey of those seeking answers about MS diagnosis, offering a ray of hope and practical advice.With a background in healthcare advocacy and a passion for making complex topics relatable, Sarah's writing style ensures that everyone can access the information they need. She knows that a supportive community and reliable information can make all the difference in facing MS, and she's here to guide you every step of the way. Join Sarah on this important journey towards understanding and managing multiple sclerosis.