Multiple sclerosis is caused by inflammation in the central nervous system, which is made up of the brain, spinal cord, and optic nerves. This inflammation damages nerve cells and causes demyelination, the destruction and loss of the myelin sheath, the protective layer that surrounds nerve fibers. The myelin layer around the axons is often referred to as a “myelin sheath.”. The myelin sheath protects axons and helps accelerate nerve transmissions.
If the myelin sheath is damaged, these nerve signals will travel more slowly or be completely blocked. 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.
In multiple sclerosis, immune cells enter the brain and spinal cord and attack both myelin and the cells that produce it. When myelin is damaged, messages have a harder time getting through or can't reach them at all. That's what causes the symptoms of multiple sclerosis. 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. The myelin sheath is a protective membrane that surrounds part of certain nerve cells. Myelin also affects how fast signals travel through those nerve cells. A number of diseases and conditions, with multiple sclerosis being the most well-known, damage or destroy myelin.
Ongoing research aims to protect, repair or regenerate myelin. In the case of multiple sclerosis, it attacks the myelin sheath in the brain and spinal cord. This is the layer that surrounds nerves, protecting them and helping electrical signals to travel from the brain to the rest of the body. Myelin is the adipose tissue that surrounds and protects nerve fibers.
In multiple sclerosis, myelin is destroyed in many areas. This loss of myelin forms scar tissue called sclerosis. These areas are also called plaques or lesions. When nerves are damaged in this way, they can't conduct electrical impulses to and from the brain.
The altered, robust and specific innate immune response of GL in MS suggests that there was a complete and robust activation of iNKT with potent cellular and cytokine activities in the generation of inflammatory demyelination. A possible subsequent step, the resolution of lesions by regulatory mechanisms and remyelination, is discussed separately (see below). In addition to the main P0 glycoprotein, the compact myelin of the PNS contains peripheral myelin protein 22 (PMP2), which represents less than 5% of the total protein. T cell subsets (Th1, Th2, Th17, CD8+, NKT, CD4+CD25+ T regulatory cells) and B cells are involved in this disorder, so new therapies for MS seek to prevent damage by restoring multiple components of the immune system.
These studies revealed that astrocytes exposed to TGF-ß1 restricted the maturation of OPCs, suggesting that canonical Notch 1 signaling is involved in adult CNS remyelination (Figure 4A). Sphingomyelin is more enriched in the myelin of peripheral nerves, where it represents 10 to 35% of total lipids, than in cerebral myelin, where it represents only 3 to 8% of the lipids. In EAE, Notch 1 appears to block remyelination, although it has not been demonstrated whether Jagged 1 is the responsible Notch 1 ligand. The next frontier aims to slow the progression of the disease and recover lost neurological function through MS therapy and, finally, to develop agents that directly affect myelin repair.
This suggests that lymphocyte reactivity, and especially that involving inflammation, should be explored with respect to the failure or severe limitation of remyelination, the process that should repair inflammatory demyelination. It prevents myelin-forming cells from attaching to axons, resulting in a reduced rate of myelination. Myelin is a fatty substance that surrounds and insulates axons (or nerve fibers) in the same way that insulation does an electrical cable. The gaps in myelin are caused by the formation of Ranvier's “nodes”, which are axonal segments where sodium channels that regulate the conduction of electrical impulses are aggregated (Figure 2B).
P2 can serve as a lipid transporter and could therefore participate in the assembly, remodeling and maintenance of myelin. In addition, the relationship between demyelination and axonal transection remains unclear, and this is particularly important as the latter is reported to underlie the permanent disability observed later in the course of the disease. It is important to recognize the differences between developmental myelination and myelin repair in the adult CNS. The subsequent sequential stages of maturation of myelinating oligodendrocytes are identified by cell-type-specific markers (Figure 2A).