myelin sheath

In an unexpected discovery, scientists working to understand the biological underpinnings of brain tumors found that increasing the activity of a protein receptor called PDGFRA reduces the production of myelin — the fatty coating that is lost in multiple sclerosis (MS) — in the nervous system. “We saw that…

A signaling protein called fractalkine helps to regulate the development of oligodendrocytes, cells of the nervous system responsible for making myelin — the protecting coating of nerve cell fibers that is damaged and lost in multiple sclerosis (MS). This finding was in the study, “Fractalkine signaling regulates…

The enzyme TET1, which is progressively lost with age, is essential to activate genes needed to repair myelin — the sheath around nerve cells that is damaged in people with multiple sclerosis (MS) — a study in mice has found. The…

A new 3D model of the human nervous system is meant to mimic key processes in the development of the myelin sheath — the fatty coating around nerve cells that is damaged in multiple sclerosis (MS) — to help with research into treatments that promote myelination. This model might also…

New research in mice suggests that poor recycling of cholesterol in the brain impairs the repair of myelin, the protective coat surrounding nerve cells that is lost in multiple sclerosis (MS). Pharmacological stimulation of cholesterol synthesis by brain immune cells — called microglia — boosted the regeneration of myelin,…

Using a two-pronged approach, researchers were able to restore myelin on regenerated nerve fibers in a mouse model of optic nerve injury, which has implications for multiple sclerosis (MS) and other diseases associated with myelin loss, a study reported. The study, “…

Oral administration of N-acetylglucosamine (GlcNAc) — a natural simple sugar sold as a dietary supplement — prevents myelin degeneration and loss of motor function in a mouse model of multiple sclerosis (MS). Myelin, the protective sheath around nerve fibers that helps to speed transmission of signals between nerve cells, is damaged…

A pathway controlled by three proteins — Daam2, Nedd4, and VHL — was identified by researchers as a key regulator of myelin production during central nervous system development and regeneration after injury. Myelin, the protective fatty layer that covers nerve fibers and helps to speed transmission of signals between nerve cells,…

Chemical modification of the protein eukaryotic elongation factor 1A1 (eEF1A1) regulates remyelination, a new study suggests, indicating that the processes regulating this protein may provide useful therapeutic targets for multiple sclerosis (MS). The study, “EEF1A1 deacetylation enables transcriptional activation of remyelination,” was published in Nature Communications.

Neuroscientist Ian D. Duncan has been awarded the 2020 John Dystel Prize for Multiple Sclerosis Research for work that advanced understanding of how myelin, the protective sheath surrounding nerve cells, can be repaired in diseases like multiple sclerosis (MS). “Professor Duncan has made a series of critical research advances…

Ursolic acid, a compound found in some herbs and in the peels of certain fruits, promoted nerve cell repair and restored the myelin sheath covering and protecting nerve endings in a mouse model of multiple sclerosis (MS), a study reported. Due to its strong anti-inflammatory and immunomodulatory…

Continuous production of fatty molecules (lipids) is crucial to the maintenance of the myelin sheath that wraps nerve fibers to protect them, ensuring the transmission of electrical impulses between nerve cells, a study reported. These findings may have strong implications for treating disorders caused by myelin loss, including…

Pheno Therapeutics, a spin-off from the University of Edinburgh, in Scotland, will search for new molecules capable of inducing the body to repair or replace the myelin sheath that is damaged in multiple sclerosis (MS). In MS, the body’s own immune system mistakes…

Blocking a protein called PAR1 may enhance the regeneration of myelin, the protective fatty layer that covers nerve fibers and is damaged in multiple sclerosis (MS), a mouse study shows. Therapeutic targeting of PAR1 may promote remyelination and delay MS progression, according to the study, “Blocking the Thrombin Receptor…

Two potassium ion channels located at gaps between segments of myelin are required for high frequency and high-speed conduction of electrical impulses along myelin-rich nerves, a study shows. Loss of the workings of these potassium channels in what are called the nodes of Ranvier slowed nerve conduction, and impaired the sensory response of a rat. These findings suggest that similar problems with these channels may exist in people with multiple sclerosis (MS). The study “TREK-1 and TRAAK Are Principal K+ Channels at the Nodes of Ranvier for Rapid Action Potential Conduction on Mammalian Myelinated Afferent Nerves” was published in the journal Neuron. Myelin, the fat-rich substance that wraps around nerve fibers (axons), works to insulate and increase the velocity of the signals relayed by nerve cells. Gaps between segments of myelin, or nodes of Ranvier, also work to amplify these signals. Nerve impulses must travel and arrive at relay points extremely quickly for effective connection and communication between brain regions. Researchers at the University of Alabama at Birmingham (UAB) showed for the first time that the nodes of Ranvier have potassium channels that allow the myelinated nerves to propagate nerve impulses at very high frequencies, and with high conduction speeds. This is key for fast transmission of sensations and rapid muscle control in mammals. The nodes of Ranvier were first discovered in 1878 by the French scientist Louis-Antoine Ranvier. Later research, dating from 1939, showed that they work as relay stations placed along myelinated nerves — about 1 millimeter apart — for proper conduction of nerve impulses at rates of 50 to 200 meters per second. Between these nodes, the nerve is wrapped in myelin. When the nerve fires, the electrical impulse travels along the nerve (called action potential) from one node to the other at a speed 100 times faster than that of impulses in nerves lacking myelin. Neuroscientists know that ions crossing the membrane of nerve cells are required to fire electrical impulses along nerves, but whether potassium ion channels were present in the nodes of Ranvier remained a matter of debate. No one had been able to use patch clamps — a technique that allows recording of whole-cell or single-ion channel currents flowing across membranes — to the nodes of the small intact nerves in mammals. UAB researchers led by Jianguo Gu, PhD, worked with a rat and identified two ion channels, called TREK-1 and TRAAK, as the main potassium channels in the nodes of Ranvier of the rat’s myelinated nerve. Most importantly, they showed these ion channels allow high-speed and high frequency conduction of nerve impulses along the myelinated afferent nerves — those carrying information from the sensory organs (like the eyes or skin) to the central nervous system (the brain and spinal cord). TREK-1 and TRAAK channels were highly enriched — 3,000 times higher — at the nodes of Ranvier in afferent nerves than in the nerve cell’s body. When the scientists removed (knocked down) these channels, conduction speed in the rat's nerve dropped by 50 percent, and the rat's "aversion reaction" to its whisker being flicked was slower. "TREK-1 and TRAAK are clustered at nodes of Ranvier of myelinated afferent nerves," the researchers concluded, and "suppressing these channels retards nerve conduction and impairs sensory functions." Increasing evidence shows that dysfunction in the nodes of Ranvier are present in neurological diseases, including MS. Whether autoantibodies (antibodies that attack the body’s own tissues) target the TREK-1 and TRAAK to affect nerve conduction, leading to sensory and motor problems such as those seen in MS, remains to be investigated, Gu said in a UAB news release written by Jeff Hansen.

Brain inflammation in multiple sclerosis (MS) hijacks immature myelin repair cells, not only preventing myelin restoration but also promoting sustained inflammation and immune attacks against myelin, a preclinical study shows.

A subset of stem cells in hair follicles, called melanocytes, appear to do more than just give rise to mature melanocytes, cells that help to determine hair color. Those melanocyte stem cells, or McSCs, that carry the CD34 protein were found in hair follicles from mice to differentiate into glia cells…

Oligodendrocyte precursor cells (OPCs), the cells responsible for myelin production, are unable to migrate into sites of myelin loss in the brain. These cells then cluster and disrupt the blood-brain barrier (BBB), triggering an inflammatory process in the early stages of multiple sclerosis (MS), a study shows. The study, “Aberrant oligodendroglial–vascular interactions disrupt the blood–brain barrier, triggering CNS inflammation,” was published in the journal Nature Neuroscience. MS is an autoimmune disease characterized by the loss of myelin (demyelination) — the fat-rich substance that protects nerve fibers — which leads to neurodegeneration. Along with loss of myelin, researchers have observed that the blood-brain barrier — a highly selective membrane that shields the central nervous system with its cerebrospinal fluid from the general blood circulation — breaks down in the initial stages of disease. A team led by researchers at the University of California, San Francisco, have now discovered that OPCs are involved in the disruption of the blood-brain barrier in MS, according to a press release from the National MS Society, which funded the study. Oligodendrocytes are myelin-producing cells and are responsible for myelinating the nerve cells’ axons — a single oligodendrocyte is capable of myelinating multiple axons. Mature myelin-producing oligodendrocytes develop from more immature, stem cell-like OPCs. In a normal brain, upon myelin loss, OPCs are called into action and travel into the damage site where they mature and generate myelin-producing oligodendrocytes. In this study, the researchers found that OPCs in MS form clusters in blood vessels of the brain-blood barrier, having lost the ability to detach from these vessels and migrate to injury sites. In an animal model of MS, they saw that OPC aggregates altered the location of other cells — called astrocytes — in a competition for space, and contributed to the disruption of blood vessels. Astrocytes are a group of star-shaped cells, belonging to the group of glial cells, that provide neurons with energy, and work as a platform to clean up their waste. They also have other functions within the brain, such as regulating blood flow and inflammation. The team also observed that OPC aggregates trigger an immune inflammatory response, shown by a large number of microglia (the central nervous system immune cells) and immune cells called macrophages around these cell clusters. “We find in several MS cases, in lesion areas with active inflammation, that OPCs can be found clustered on vasculature, representing a defect in single cell perivascular migration and inability to detach from blood vessels,” the researchers wrote. Further molecular analysis revealed that OPCs have high levels of Wnt signaling, and elevated secretion of Wif1 factor to the extracellular space that could explain why OPCs accumulate and destroy the blood-brain barrier. The WiF1 factor is actually a negative regulator of Wnt signaling that is essential for the maintenance of the blood-brain barrier structure. This factor competes with Wnt ligands, and affects the integrity of cellular junctions, making the blood-brain barrier more fragile and permeable. "Evidence for this defective oligodendroglial–vascular interaction in MS suggests that aberrant OPC perivascular migration not only impairs their lesion recruitment but can also act as a disease perpetuator via disruption of the BBB,” the researchers wrote. They suggested that more studies are needed to better understand the interactions between blood vessels and oligodendrocytes, which could help identify new therapeutic targets for promoting myelin repair in MS.

A shortened DNA molecule showed an increased ability to bind myelin in human cells, and may boost the development of remyelination approaches for multiple sclerosis (MS) treatment, according to a study. The study, “Optimization of a 40-mer Antimyelin DNA Aptamer Identifies a 20-mer with Enhanced Properties…

Schwann cells surrounding neurons protect the degeneration of nerves by blocking thrombin, a blood-clotting protein that can also damage nerves, according to a new study. These findings may aid in the further understanding of genetic and molecular mechanisms behind conditions such as multiple sclerosis (MS). Results of the study, “Glial cells…

Unusually high levels of a transcription factor called paired related homeobox protein 1 (PRRX1) in human oligodendrocyte progenitor cells hinders their ability to respond to the loss of myelin and to transform into mature, myelin-producing oligodendrocytes, a new study shows. These findings suggest a new potential way of treating …

The formation of new myelin sheaths by oligodendrocytes is impaired in the absence of a small molecule, called Vav3, that oversees pathways regulating the shape of oligodendrocytes, new study reports. Its researchers pinpoint Vav3 as a potential therapeutic target to improve and speed myelin repair in diseases like multiple sclerosis…

Mature, adult oligodendrocytes can reacquire their ability to produce myelin to replace the ones lost in diseases like multiple sclerosis (MS) without undergoing a stem cell-like state, a new study shows. Myelin is the fat-rich substance that wraps around nerve fiber projections (axons) protecting them and increasing the speed of…

A molecule known as Sox10 enables brain cells called astrocytes to convert into myelin-forming oligodendrocytes, a new study in mice reports. The findings suggest an approach for myelin repair in patients with multiple sclerosis (MS) and similar disorders, its researchers said. The study, “In vivo conversion of…

A better understanding of the processes behind a continual and healthy renewal of myelin — the fatty, protective substance wrapping nerve cell fibers — may now exist. Researchers identified an enzyme, called PRMT5, that they believe regulates the number of myelin-producing cells in the brain and spinal cord. Their discovery…

Blocking a protein receptor called muscarinic type 3 (M3R) could be an effective way to promote remyelination in multiple sclerosis (MS) patients, according to a State University of New York at Buffalo (UB) study in mice. The research, “Muscarinic receptor M3R signaling prevents efficient remyelination by…

Inhibiting an oxidative stress enzyme called myeloperoxidase protects the blood-brain barrier in a mouse model of multiple sclerosis (MS), limiting the migration of immune cells and halting their attack on nerve cells, researchers have found. Disruption of the blood-brain barrier is a hallmark of various disorders, including MS, and when…

A chemical compound called indazole chloride promotes repair of myelin, the protective layer of nerve fibers, through “beneficial” inflammation in a mouse model of multiple sclerosis (MS), a study reports. The preclinical research, “Increase in chemokine CXCL1 by ERβ ligand treatment is a key mediator in…

A molecule responsible for preventing the repair of white matter in the brain, a process critical to treating multiple sclerosis (MS) and cerebral palsy, has been identified. The research, “A TLR/AKT/FoxO3 immune-tolerance like pathway disrupts the repair capacity of oligodendrocyte progenitors,” was published in The Journal…

Subtle changes in myelin, the protective layer of nerve fibers, may be an early event in multiple sclerosis (MS) prior to the inflammatory reaction, a new University of Calgary study shows. The study, “Biochemically altered myelin triggers autoimmune demyelination,” was published in the journal Proceedings…