myelin

Measuring the speed of signals sent to the brain by nerves in the eye could help assess if remyelination is taking place, a study in cats suggests. Such measurements could be useful in evaluating multiple sclerosis (MS) treatments aiming to repair myelin in clinical trials — of particular interest…

MetP Pharma‘s patent application for a new method to treat demyelinating and neuroinflammatory diseases, including multiple sclerosis (MS), has been approved by the United States Patent and Trademark Office (USPTO). The patent, titled “Treatment of Demyelinating Diseases” (U.S. Appl. No. 16/506,830), is valid until 2039,…

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.

The National Multiple Sclerosis Society awarded more than $339,000 to Clene Nanomedicine to support clinical tests into its lead candidate CNM-Au8 in treating multiple sclerosis (MS) by protecting nerve cells and restoring myelin. The grant was awarded under the National MS Society’s Fast Forward program, which aims…

Metformin, a common diabetes treatment that works to mimic dietary fasting, was seen to promote remyelination in the stem cells of elderly rats, suggesting it may be useful in treating multiple sclerosis. “Metformin Restores CNS Remyelination Capacity by Rejuvenating Aged Stem Cells” was published in…

Blocking production of the low-density lipoprotein receptor-related protein 1 (LRP1) — involved in inflammatory and immune responses — specifically in myelin repair cells halts neuroinflammation and promotes myelin repair, a preclinical study shows. These results, from two mouse models of multiple sclerosis (MS), shed light on the underlying mechanisms…

A protein known as nuclear factor I-A (NFIA) is key for spinal cord repair and timely remyelination by astrocytes — the most abundant cells in the brain and first responders to sites of injury, findings in a mouse model of multiple sclerosis (MS) suggest. In brain lesions, NFIA is…

A diagnosis of multiple sclerosis (MS) often leaves patients and their families with many unanswered questions. It can be hard to find information, connect with other patients, and find support. Here are some frequently asked questions and answers about MS: What is MS? MS is an autoimmune disease —…

NervGen Pharma announced plans to open clinical trials evaluating the potential of its lead candidate NVG-291 to treat multiple sclerosis (MS) and spinal cord injury. NVG-291 is an investigational peptide that has shown an ability to stimulate nerve regeneration following an injury in several animal models of disease.

Ofatumumab Better at Easing Relapse Rates and Slowing MS Progression Than Aubagio, Phase 3 Data Show Ofatumumab isn’t approved as a multiple sclerosis (MS) treatment. It’s a cancer medication that’s marketed as Arzerra. But in two clinical trials reported here, it did better than Aubagio at treating MS. Its…

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.

Higher levels of vitamin D in the blood may help to protect the myelin sheath, slowing damage to nerve cells in people with progressive forms of multiple sclerosis (MS), a brain imaging study reports. The study, “Vitamin D and MRI measures in progressive multiple sclerosis,” was published in the…

Two new studies delve into the structure of SARM1, an enzyme that plays a key role in nerve cell degeneration, and are expected to aid the development of targeted therapies for neurodegenerative disorders such as multiple sclerosis (MS), amyotrophic lateral sclerosis (ALS), and peripheral neuropathies. SARM1…

Our brains — much like our joints — stiffen with age, causing brain stem cells called oligodendrocyte progenitor cells (OPCs) to lose their ability to proliferate and transform into oligodendrocytes, the cells that produce myelin, an essential component for nerve cell communication, a study found. But tricking OPCs into sensing a…

SyntheticMR‘s SyMRI NEURO, a software package that can segment and measure myelin volume in the brain, is now available for use by radiologists in the U.S. through an agreement with Siemens Healthineers and its syngo.via magnetic resonance imaging (MRI) visualization platform, a press release states. SyMRI NEURO’s integrated software package…

The development of new medicines to treat myelin-related neurological diseases, such as multiple sclerosis (MS), has been given a boost by a €2.9 million (about $3.2 million) research grant awarded to the Belgian biotech company Rewind Therapeutics by…

Projection neurons, a specific type of nerve cell, are prone to damage in the brain of people with multiple sclerosis (MS), and could be at the root of brain atrophy (shrinkage) and the cognitive changes seen in patients. Looking at individual cells in the brain, scientists found…

Convelo Therapeutics has announced a collaboration with Genentech, a member of the Roche Group, to work toward the development of new remyelination therapies for multiple sclerosis (MS) and other myelin disorders. “We are excited to be working with Genentech to…

Treating people with relapsing forms of multiple sclerosis (MS) with opicinumab and Avonex (interferon beta-1a) for 72 weeks did not lead to a dose-dependent reduction in disability,  results of a Phase 2 trial show. However, an ongoing study is evaluating opicinumab in a subgroup with better clinical responses.

A new study demonstrates that intracellular sigma peptide (ISP) can promote remyelination in a mouse model of multiple sclerosis (MS). Importantly, this study was independent of NervGen, a pharmaceutical company that is developing an ISP-like compound — NVG-291 — for the treatment of nerve injury and MS. The study,…

NervGen wants to advance the development of NVG-291, its lead investigational therapy for spinal cord damage, as a potential remyelination treatment for multiple sclerosis (MS), the company announced. Following preclinical data showing that NVG-291 promotes myelin repair and regeneration of damaged nerves in animal models of…

A protein leads to nerve fiber and myelin damage, particularly in progressive forms of multiple sclerosis, by activating brain immune cells called microglia, according to a new study. Its researchers also noted this protein is the target of experimental MS treatment called temelimab (GNbAC1), which showed potential in Phase 2 clinical trials. The…

Editor’s note: “Need to Know” is a series inspired by common forum questions and comments from readers. Have a comment or question about MS? Visit our forum. This week’s question is inspired by the forum topic “How the Blood Brain Barrier May Thwart MS Progression” from Feb. 9, 2017. What…

Exosomes — tiny vesicles secreted by cells — collected from bone marrow stem cells and injected into a mouse model of multiple sclerosis (MS) helped to treat the disease, a study reports. Specifically, this treatment eased myelin loss and neuroinflammation in the mice, and improved motor function, the…

Treatment with Mayzent (siponomod) may reduce myelin deterioration by lessening the accumulation of immune cells in brain meninges, and preventing the migration of pro-inflammatory lymphocytes into the brain, according to a study in a mouse model of multiple sclerosis (MS). The research, “A Mouse Model of…

Giving estrogen to two different adult mouse models of multiple sclerosis (MS), including the experimental autoimmune encephalomyelitis (EAE) model, promoted remyelination, a new study shows. Exposure to the hormone affected gene activity in oligodendrocytes, tricking them into producing myelin (the fatty substance that protects nerve cells, and that is destroyed…

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…

Cellular senescence — the process of aging at the cellular level — may play a role in the development of primary progressive multiple sclerosis (PPMS) by limiting the ability of myelin-producing cells (oligodendrocytes) to renew and mature. The study with that finding, “Cellular senescence in progenitor…

Researchers have developed a compound based on the thyroid hormone T3 that is able to repair damaged myelin in the brain of mice, a discovery that holds promise for healing myelin loss in patients with multiple sclerosis (MS), results of an early study reveal.

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.