Where is myelin research being done

Local recruitment of remyelinating cells in the repair of demyelination in the central nervous system. Frischer, J. Clinical and pathological insights into the dynamic nature of the white matter multiple sclerosis plaque. Fumagalli, M. Pharmacological properties and biological functions of the GPR17 receptor, a potential target for neuro-regenerative medicine. Glycolytic oligodendrocytes maintain myelin and long-term axonal integrity.

Gibson, E. Neuronal activity promotes oligodendrogenesis and adaptive myelination in the mammalian brain. Science Giraudon, P. Semaphorin CD from activated T lymphocytes induces process extension collapse in oligodendrocytes and death of immature neural cells. Goldschmidt, T. Remyelination capacity of the MS brain decreases with disease chronicity. Green, A. Clemastine fumarate as a remyelinating therapy for multiple sclerosis ReBUILD : a randomised, controlled, double-blind, crossover trial.

Lancet , — Griffiths, I. Axonal swellings and degeneration in mice lacking the major proteolipid of myelin. Science , — Gudi, V. Regional differences between grey and white matter in cuprizone induced demyelination.

Brain Res. Guglielmetti, C. Neuroimage 86, 99— Hammond, T. Single cell RNA sequencing of microglia throughout the mouse lifespan and in the injured brain reveals complex cell-state changes. Immunity 50, — Harlow, D.

Harsan, L. Recovery from chronic demyelination by thyroid hormone therapy: myelinogenesis induction and assessment by diffusion tensor magnetic resonance imaging. Harty, B. Myelinating Schwann cells ensheath multiple axons in the absence of E3 ligase component Fbxw7.

Hasan, M. Schema-like learning and memory consolidation acting through myelination. Hawryluk, G. An examination of the mechanisms by which neural precursors augment recovery following spinal cord injury: a key role for remyelination. Hefendehl, J. Homeostatic and injury-induced microglia behavior in the aging brain.

Aging Cell 13, 60— Lesion stage-dependent causes for impaired remyelination in MS. Hinks, G. Delayed changes in growth factor gene expression during slow remyelination in the CNS of aged rats. Huang, J. Retinoid X receptor gamma signaling accelerates CNS remyelination. Hubler, Z. Accumulation of 8,9-unsaturated sterols drives oligodendrocyte formation and remyelination.

Imitola, J. Genomics 14, — Irvine, K. Remyelination protects axons from demyelination-associated axon degeneration. Itoyama, Y. Spinal cord multiple sclerosis lesions in Japanese patients: Schwann cell remyelination occurs in areas that lack glial fibrillary acidic protein GFAP. Schwann cell remyelination of demyelinated axons in spinal cord multiple sclerosis lesions.

Jablonska, B. Chordin-induced lineage plasticity of adult SVZ neuroblasts after demyelination. Jagielska, A. Mechanical strain promotes oligodendrocyte differentiation by global changes of gene expression. Mechanical environment modulates biological properties of oligodendrocyte progenitor cells.

Cells Dev. Juurlink, B. Peroxide-scavenging deficit underlies oligodendrocyte susceptibility to oxidative stress. Glia 22, — Karimi-Abdolrezaee, S.

Delayed transplantation of adult neural precursor cells promotes remyelination and functional neurological recovery after spinal cord injury. Kazanis, I. Subependymal zone-derived oligodendroblasts respond to focal demyelination but fail to generate myelin in young and aged mice. Keirstead, H. Identification of post-mitotic oligodendrocytes incapable of remyelination within the demyelinated adult spinal cord. The role of oligodendrocytes and oligodendrocyte progenitors in CNS remyelination.

Keough, M. An inhibitor of chondroitin sulfate proteoglycan synthesis promotes central nervous system remyelination. Keren-Shaul, H. A unique microglia type associated with restricting development of Alzheimer's disease. Cell , — Klistorner, A. Assessment of opicinumab in acute optic neuritis using multifocal visual evoked potential. CNS Drugs 32, — Kremer, D. Human endogenous retrovirus type W envelope protein inhibits oligodendroglial precursor cell differentiation.

Kuhlmann, T. An updated histological classification system for multiple sclerosis lesions. Differentiation block of oligodendroglial progenitor cells as a cause for remyelination failure in chronic multiple sclerosis. Lampron, A. Inefficient clearance of myelin debris by microglia impairs remyelinating processes. Lappe-Siefke, C. Disruption of Cnp1 uncouples oligodendroglial functions in axonal support and myelination. Lariosa-Willingham, K. A central nervous system axonal myelination assay for high-throughput screening.

Methods Mol. Lau, L. Pathophysiology of the brain extracellular matrix: a new target for remyelination. Chondroitin sulfate proteoglycans in demyelinated lesions impair remyelination. Ann Neurol. Lecca, D. The recently identified P2Y-like receptor GPR17 is a sensor of brain damage and a new target for brain repair. Lee, Y. Oligodendroglia metabolically support axons and contribute to neurodegeneration. Lentferink, D.

Levine, J. Activation and proliferation of endogenous oligodendrocyte precursor cells during ethidium bromide-induced demyelination. Li, Z. Clemastine rescues behavioral changes and enhances remyelination in the cuprizone mouse model of demyelination. Liddelow, S.

Neurotoxic reactive astrocytes are induced by activated microglia. Lloyd, A. Central nervous system regeneration is driven by microglia necroptosis and repopulation. The pro-remyelination properties of microglia in the central nervous system.

Lois, C. To investigate whether SVZ cells from adult mice could differentiate into neurons. Lombardi, M. Detrimental and protective action of microglial extracellular vesicles on myelin lesions: astrocyte involvement in remyelination failure. Lucchinetti, C. A quantitative analysis of oligodendrocytes in multiple sclerosis lesions. A study of cases. Heterogeneity of multiple sclerosis lesions: implications for the pathogenesis of demyelination.

Macchi, M. Mature oligodendrocytes bordering lesions limit demyelination and favor myelin repair via heparan sulfate production. Elife Magalon, K. Enriched environment promotes adult neural progenitor cell mobilization in mouse demyelination models.

Olesoxime favors oligodendrocyte differentiation through a functional interplay between mitochondria and microtubules. Neuropharmacology , — Olesoxime accelerates myelination and promotes repair in models of demyelination. Magliozzi, R. Inflammatory intrathecal profiles and cortical damage in multiple sclerosis: intrathecal inflammation in MS. Makhija, E. Mechanical regulation of oligodendrocyte biology. Marques, S. Oligodendrocyte heterogeneity in the mouse juvenile and adult central nervous system.

McKenzie, I. Motor skill learning requires active central myelination. McMurran, C. CNS remyelination and the innate immune system. Mecha, M. The endocannabinoid 2-AG enhances spontaneous remyelination by targeting microglia. Brain Behav. Involvement of Wnt7a in the role of M2c microglia in neural stem cell oligodendrogenesis.

Mei, F. Micropillar arrays as a high-throughput screening platform for therapeutics in multiple sclerosis. Accelerated remyelination during inflammatory demyelination prevents axonal loss and improves functional recovery. Menn, B. Origin of oligodendrocytes in the subventricular zone of the adult brain. Mercier, F. Fractones: extracellular matrix niche controlling stem cell fate and growth factor activity in the brain in health and disease.

Life Sci. Merkle, F. Adult neural stem cells in distinct microdomains generate previously unknown interneuron types. Mi, S. LINGO-1 negatively regulates myelination by oligodendrocytes.

CNS Drugs 27, — Miron, V. M2 microglia and macrophages drive oligodendrocyte differentiation during CNS remyelination. Mirzadeh, Z. Neural stem cells confer unique pinwheel architecture to the ventricular surface in neurogenic regions of the adult brain. Cell Stem Cell 3, — Montag, D. Mice deficient for the myelin-associated glycoprotein show subtle abnormalities in myelin.

Neuron 13, — Moyon, S. Demyelination causes adult CNS progenitors to revert to an immature state and express immune cues that support their migration.

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Nait-Oumesmar, B. Progenitor cells of the adult mouse subventricular zone proliferate, migrate and differentiate into oligodendrocytes after demyelination.

Activation of the subventricular zone in multiple sclerosis: evidence for early glial progenitors. Najm, F. Drug-based modulation of endogenous stem cells promotes functional remyelination in vivo.

Napoli, I. Protective effects of microglia in multiple sclerosis. Nave, K. Myelination and support of axonal integrity by glia. Neumann, B. Metformin restores CNS remyelination capacity by rejuvenating aged stem cells. Cell Stem Cell 25, — Problems and pitfalls of identifying remyelination in multiple sclerosis. Stem Cell 26, — Nissen, J. Csf1R inhibition attenuates experimental autoimmune encephalomyelitis and promotes recovery. Nyamoya, S. G-protein-coupled receptor Gpr17 expression in two multiple sclerosis remyelination models.

Ohgoh, M. Altered expression of glutamate transporters in experimental autoimmune encephalomyelitis. O'Loughlin, E. Microglial phenotypes and functions in multiple sclerosis. Omari, K. CXC chemokine receptors on human oligodendrocytes: implications for multiple sclerosis. Orthmann-Murphy, J. Remyelination alters the pattern of myelin in the cerebral cortex. Ortiz, F. Neuronal activity in vivo enhances functional myelin repair. JCI Insight Pan, S.

Preservation of a remote fear memory requires new myelin formation. Patani, R. Remyelination can be extensive in multiple sclerosis despite a long disease course. Patrikios, P. Other drugs that may reduce fatigue include amantadine, methylphenidate, and modafinil. Occupational therapy can help people learn how to walk using an assistive device or in a way that saves physical energy. Stress management programs, relaxation training, membership in an MS support group, or individual psychotherapy may help some people.

Pain from MS can be felt in different parts of the body. Trigeminal neuralgia facial pain is treated with anticonvulsant or antispasmodic drugs, or less commonly painkillers. Treatments for chronic back or other musculoskeletal pain may include heat, massage, ultrasound, and physical therapy. Problems with bladder control and constipation may include urinary frequency, urgency, or the loss of bladder control. A small number of individuals retain large amounts of urine. Medical treatments are available for bladder-related problems.

Constipation is also common and can be treated with a high-fiber diet, laxatives, and stool softeners. Sexual dysfunction can result from damage to nerves running through the spinal cord. Sexual problems may also stem from MS symptoms such as fatigue, cramped or spastic muscles, and psychological factors. Some of these problems can be corrected with medications. Psychological counseling also may be helpful. C linical depression is frequent among people with MS.

MS may cause depression as part of the disease process and chemical imbalance in the brain. Depression can intensify symptoms of fatigue, pain, and sexual dysfunction.

It is most often treated with cognitive behavioral therapy, and selective serotonin reuptake inhibitor SSRI antidepressant medications, which are less likely than other antidepressant medications to cause fatigue.

Inappropriate and involuntary expressions of laughter, crying, or anger —symptoms of a condition called pseudobulbar affect—sometimes are associated with MS. These expressions are often incongruent with mood; for example, people with MS may cry when they are actually happy or laugh when they are not especially happy.

The combination treatment of the drugs dextromethorphan and quinidine can treat pseudobulbar affect, as can other drugs such as amitriptyline or citalopram.

Cognitive impairment —a decline in the ability to think quickly and clearly and to remember easily—affects up to three-quarters of people with MS. These cognitive changes may appear at the same time as the physical symptoms or they may develop gradually over time.

Drugs such as donepezil may be helpful in some cases. Many people with MS benefit from complementary or alternative approaches such as acupuncture, aromatherapy, ayurvedic medicine, touch and energy therapies, physical movement disciplines such as yoga and tai chi, herbal supplements, and biofeedback. Because of the risk of interactions between alternative and conventional therapies, people with MS should discuss all the therapies they are using with their doctor, especially herbal supplements.

Herbal supplements have biologically active ingredients that could have harmful effects on their own or interact harmfully with other medications. Although researchers have not been able to identify the cause of MS with any certainty, there has been excellent progress in other areas of MS research—especially in the development of new treatments to prevent exacerbations of the disease.

New discoveries are constantly changing MS treatment options and helping to reduce MS-related disability. Research projects being conducted by NINDS scientists or through NIH grants to universities and other sites throughout the United States cover a wide range of topics such as comorbidities, mechanisms of cognitive impairment, blood-brain barrier breakdown in MS, the role of sleep and circadian rhythms, rehabilitation strategies, and telehealth.

Other topics include:. For more information about BEAT-MS and how to apply to participate in this study or other clinical studies, visit www. Genetic research funded by NINDS is exploring the roles of "susceptibility genes"—genes that are associated with an increased risk for MS. Several candidate genes have been identified and researchers are studying their function in the nervous system to discover how they may lead to the development of MS.

Other studies aim to develop better neuroimaging tools , such as more powerful MRI methods, to diagnose MS, track disease progression, and assess treatments. NINDS scientists are collecting magnetic resonance imaging of the brain and spinal cord and scans of the retina, along with other clinical and biological data, from more than individuals with MS and 50 individuals without the disease over a period of years to observe changes in the course of MS over time.

Investigators also are using MRI to study the natural history of MS and to help define the mechanism of action and cause of side effects of disease modifying therapies. NIH supports translational studies to develop therapies that will stop or reverse the course of the disease, focusing on pathways that modify immune system function, repair damaged myelin, or protect neurons from damage.

Three neurons credit: Daniel Berger and Giulio Tomassy. What this means, Arlotta said, is that the higher in the cerebral cortex one looks — the closer to the top of the brain, which is its most evolved region — the less myelin one finds. In classic neurobiology textbooks, myelin is represented on axons as a sequence of myelinated segments separated by very short nodes that lack myelin. This distribution of myelin was assumed to be always the same, on every neuron, from the beginning to the end of the axon.

A study shows that myelin loss may contribute to neurodegeneration in a mouse model of Alzheimer disease. Dong and colleagues investigated mechanisms mediating neurodegeneration in multiple sclerosis and identified a direct role for oxidized phosphatidylcholines OxPCs in driving CNS cell death. Three new studies show that activity-dependent formation of myelin contributes to memory consolidation and recall, possibly by increasing functional coupling between neuronal ensembles encoding experience.

Research Highlights 27 August The 15q Research Highlights 05 June Dysregulation of adaptive myelination might contribute to methotrexate chemotherapy-related cognitive impairment in mice. Advanced search. Skip to main content Thank you for visiting nature. Atom RSS Feed Myelin biology and repair Definition Myelin biology and repair refers to the science of myelin physiology, manufacture, and how myelin damage in either the peripheral or central nervous systems can be repaired.

Related Subjects Multiple sclerosis.