What Is Myelin? | National Multiple Sclerosis Society

• Myelin and Multiple Sclerosis
• Immune-Mediated Disease and MS
• Demyelination and Multiple Sclerosis

New Hope in Myelin Repair

Stem cell therapies show early successes in lab models. 
 

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In this article

Overview of myelin and multiple sclerosis

Myelin is a fatty substance that surrounds and insulates axons (or nerve fibers) much as insulation does an electrical wire. It is an electrical conductor composed mostly of lipids, water and proteins.

Myelin is present in the central nervous system and peripheral nervous system. However, only the central nervous system is affected by multiple sclerosis. Central nervous system myelin is produced by special cells called oligodendrocytes.

Myelin sheath function

The coating of myelin around axons is often referred to as a “myelin sheath.” The myelin sheath protects the axons and helps speed nerve transmissions. If the myelin sheath is damaged, these nerve signals will travel more slowly or be blocked completely.

Abnormal immune response and multiple sclerosis

Our immune systems are responsible for protecting our bodies from infection. In MS, something triggers the immune system to attack the central nervous system. This attack produces inflammation and:

• Damages or destroys myelin and oligodendrocytes (a process referred to as demyelination)
• Causes damage to the axons
• Produces damaged areas (lesions or scars) along the nerve, which can be detected on magnetic resonance imaging (MRI)
• Slows or halts nerve conduction — producing the neurologic signs and symptoms of MS

Learn more about what causes MS.

Research efforts underway to stimulate myelin repair

Scientists have discovered that the body heals some lesions naturally by stimulating oligodendrocytes in the area — or by recruiting young oligodendrocytes from further away — to begin making new myelin at the damaged site. However, this natural repair process is slow and incomplete. Scientists are investigating several different strategies for stimulating the repair of myelin. They are testing existing drugs and finding ways to stimulate oligodendrocytes to produce myelin. In addition, they are researching ways to protect oligodendrocytes and myelin from further damage.

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Advisory Committee for Pilot Glial/Myelin Research (.pdf)


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Diagnostic Workup for Patients with Suspected Demyelinating Disease – Testing Options (.pdf)


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Resources and Services for Your Patients


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Resources for You and Your Practice


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Managing MS


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Diagnosing MS


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About MS


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Primary Progressive Multiple Sclerosis (PPMS)


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Secondary Progressive Multiple Sclerosis (SPMS)


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Relapsing-remitting Multiple Sclerosis (RRMS)


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Clusters


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Viruses


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Immune-Mediated Disease and MS


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Pediatric Multiple Sclerosis


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Multiple sclerosis: MedlinePlus Medical Encyclopedia

Multiple sclerosis (MS) is an autoimmune disease that affects the brain and spinal cord (central nervous system).

MS affects women more than men. The disorder is most commonly diagnosed between ages 20 to 40, but it can be seen at any age.

MS is caused by damage to the myelin sheath. This sheath is the protective covering that surrounds nerve cells. When this nerve covering is damaged, nerve signals slow or stop.

The nerve damage is caused by inflammation. Inflammation occurs when the body’s own immune cells attack the nervous system. This can occur along any area of the brain, optic nerve, and spinal cord.

It is unknown what exactly causes MS. The most common thought is that it is caused by a virus, a gene defect, or both. Environmental factors may also play a role.

You are slightly more likely to develop this condition if you have a family history of MS or you live in a part of the world where MS is more common.

Symptoms vary because the location and severity of each attack can be different. Attacks can last for days, weeks, or months. Attacks are followed by remissions. These are periods of reduced symptoms or no symptoms. Fever, hot baths, sun exposure, and stress can trigger or worsen attacks.

Nerves in any part of the brain or spinal cord may be damaged. Because of this, MS symptoms can appear in many parts of the body.

Muscle symptoms:

• Loss of balance
• Muscle spasms
• Numbness or abnormal sensation in any area
• Problems moving arms or legs
• Problems walking
• Problems with coordination and making small movements
• Tremor in one or more arms or legs
• Weakness in one or more arms or legs

Bowel and bladder symptoms:

• Constipation and stool leakage
• Difficulty beginning to urinate
• Frequent need to urinate
• Strong urge to urinate
• Urine leakage (incontinence)

Eye symptoms:

• Double vision
• Eye discomfort
• Uncontrollable eye movements
• Vision loss (usually affects one eye at a time)

Numbness, tingling, or pain:

• Facial pain
• Painful muscle spasms
• Tingling, crawling, or burning feeling in the arms and legs

Other brain and nerve symptoms:

• Decreased attention span, poor judgment, and memory loss
• Difficulty reasoning and solving problems
• Depression or feelings of sadness
• Dizziness and balance problems
• Hearing loss

Sexual symptoms:

• Problems with erections
• Problems with vaginal lubrication

Speech and swallowing symptoms:

• Slurred or difficult-to-understand speech
• Trouble chewing and swallowing

Fatigue is a common and bothersome symptom as MS progresses. It is often worse in the late afternoon.

Symptoms of MS may mimic those of many other nervous system problems. MS is diagnosed by determining if there are signs of more than one attack on the brain or spinal cord and by ruling out other conditions.

People who have a form of MS called relapsing-remitting MS have evidence of at least two attacks separated by a remission.

In other people, the disease may slowly get worse in between clear attacks. This form is called secondary progressive MS. A form with gradual progression, but no clear attacks is called primary progressive MS.

The health care provider may suspect MS if there are decreases in the function of two different parts of the central nervous system (such as abnormal reflexes) at two different times.

An exam of the nervous system may show reduced nerve function in one area of the body. Or the reduced nerve function may be spread over many parts of the body. This may include:

• Abnormal nerve reflexes
• Decreased ability to move a part of the body
• Decreased or abnormal sensation
• Other loss of nervous system functions, such as vision

An eye exam may show:

• Abnormal pupil responses
• Changes in the visual fields or eye movements
• Decreased visual acuity
• Problems with the inside parts of the eye
• Rapid eye movements triggered when the eye moves

Tests to diagnose MS include:

• Blood tests to rule out other conditions that are similar to MS.
• Lumbar puncture (spinal tap) for cerebrospinal fluid (CSF) tests, including CSF oligoclonal banding may be needed.
• MRI scan of the brain or the spine, or both are important to help diagnose and follow MS.
• Nerve function study (evoked potential test, such as visual evoked response) is less often used.

There is no known cure for MS at this time, but there are treatments that may slow the disease. The goal of treatment is to stop progression, control symptoms, and help you maintain a normal quality of life.

Medicines are often taken long-term. These include:

• Medicines to slow the disease
• Steroids to decrease the severity of attacks
• Medicines to control symptoms such as muscle spasms, urinary problems, fatigue, or mood problems

Medicines are more effective for the relapsing-remitting form than for other forms of MS.

The following may also be helpful for people with MS:

• Physical therapy, speech therapy, occupational therapy, and support groups
• Assistive devices, such as wheelchairs, bed lifts, shower chairs, walkers, and wall bars
• A planned exercise program early in the course of the disorder
• A healthy lifestyle, with good nutrition and enough rest and relaxation
• Avoiding fatigue, stress, temperature extremes, and illness
• Changes in what you eat or drink if there are swallowing problems
• Making changes around the home to prevent falls
• Social workers or other counseling services to help you cope with the disorder and get assistance
• Vitamin D or other supplements (talk to your provider first)
• Complementary and alternative approaches, such as acupuncture or cannabis, to help with muscle problems
• Spinal devices can reduce pain and spasticity in the legs

Living with MS may be a challenge. You can ease the stress of illness by joining an MS support group. Sharing with others who have common experiences and problems can help you not feel alone.

The outcome varies, and is hard to predict. Although the disorder is life-long (chronic) and incurable, life expectancy can be normal or almost normal. Most people with MS are active and function at work with little disability.

Those who usually have the best outlook are:

• Females
• People who were young (less than 30 years old) when the disease started
• People with infrequent attacks
• People with a relapsing-remitting pattern
• People who have limited disease on imaging studies

The amount of disability and discomfort depends on:

• How often and severe the attacks are
• The part of the central nervous system that is affected by each attack

Most people return to normal or near-normal function between attacks. Over time, there is greater loss of function with less improvement between attacks.

MS may lead to the following:

• Depression
• Difficulty swallowing
• Difficulty thinking
• Less and less ability to care for self
• Need for indwelling catheter
• Osteoporosis or thinning of the bones
• Pressure sores
• Side effects of medicines used to treat the disorder
• Urinary tract infections

Contact your provider if:

• You develop any symptoms of MS
• Your symptoms get worse, even with treatment
• The condition worsens to the point when home care is no longer possible

MS; Demyelinating disease

• Caring for muscle spasticity or spasms
• Constipation – self-care
• Daily bowel care program
• Multiple sclerosis – discharge
• Preventing pressure ulcers
• Swallowing problems

• Multiple sclerosis
• MRI of the brain
• Central nervous system and peripheral nervous system
• Myelin and nerve structure

Calabresi PA, Multiple sclerosis and demyelinating conditions of the central nervous system. In: Goldman L, Schafer AI, eds. Goldman-Cecil Medicine. 26th ed. Philadelphia, PA: Elsevier; 2020:chap 383.

Fabian MT, Krieger SC, Lublin FD. Multiple sclerosis and other inflammatory demyelinating diseases of the central nervous system. In: Jankovic J, Mazziotta JC, Pomeroy SL, Newman NJ, eds. Bradley and Daroff’s Neurology in Clinical Practice. 8th ed. Philadelphia, PA: Elsevier; 2022:chap 80.

Rae-Grant A, Day GS, Marrie RA, et al. Practice guideline recommendations summary: disease-modifying therapies for adults with multiple sclerosis: report of the Guideline Development, Dissemination, and Implementation Subcommittee of the American Academy of Neurology. Neurology. 2018;90(17):777-788. PMID: 29686116 pubmed.ncbi.nlm.nih.gov/29686116/.

Updated by: Joseph V. Campellone, MD, Department of Neurology, Cooper Medical School at Rowan University, Camden, NJ. Review provided by VeriMed Healthcare Network. Also reviewed by David Zieve, MD, MHA, Medical Director, Brenda Conaway, Editorial Director, and the A. D.A.M. Editorial team.

Ursolic acid restored the myelin sheaths of neurons in mice with sclerosis

Ursolic acid, when administered orally, stops the development of an analog of multiple sclerosis in mice, stimulates the maturation of oligodendrocytes and restores the myelin sheath of neurons of the central nervous system. The acid interacts with the gamma receptor activated by peroxisomal proliferators and, through the transcription factor CREB, triggers the release of the ciliary neurotrophic factor, which affects the differentiation of oligodendrocyte precursors. The study was published in the journal Proceedings of the National Academy of Sciences .

Multiple sclerosis is an autoimmune disease that disrupts the myelin sheath of neurons throughout the central nervous system. Modern approaches to the treatment of multiple sclerosis make it possible to stop autoimmune reactions and are effective in the early stages of the disease. However, there is no way to restore the myelin sheaths of nerve cells and return them to functionality. There is a potential for this – in the foci of demyelination, precursors of oligodendrocytes (cells that form the shells of neurons in the central nervous system) accumulate, but they do not develop.

Ursolic acid is found in many plants, including fruit peels. This substance has a whole range of pharmacological properties, it is used as part of medicinal plants for the treatment of Parkinson’s disease, rheumatoid arthritis and diabetes. The administration of ursolic acid can also prevent the development of experimental autoimmune encephalomyelitis (EAE, a mouse model of multiple sclerosis).

Chinese and US scientists led by Yuan Zhang of Thomas Jefferson University investigated the effect of ursolic acid on mice with EAE. The substance was administered orally, therapy was started at the beginning of the development of the disease (11 days after the start of the development of EAE), at its peak (18 days) or in the chronic phase (60 days). On day 30 or 120, sections of the spinal cord of mice were obtained and immunohistochemically stained for various markers (for example, myelin, axons, oligodendrocytes).

In order to separate the anti-inflammatory and myelinating effects of ursolic acid, its action was studied in mice, the destruction of myelin in the brain of which was triggered by cuprizone – in this case, inflammatory processes and the presence of immune T-cells in the lesion are minimal. In addition, the effect of ursolic acid was tested on astrocyte culture — these cells secrete oligodendrocyte development factors.

All of the studies described above were also performed in animals heterozygous for the peroxisome proliferator-activated receptor gamma (PPARγ) gene. Ursolic acid is an agonist of this receptor, and its activation alleviates inflammation and triggers neuronal defense mechanisms. The authors of the work suggested that the interaction with PPARγ is the main mechanism of action of ursolic acid.

The most effective dose of ursolic acid was found to be 25 milligrams per kilogram of body weight per day. The drug significantly reduced inflammation (p < 0. 01) and demyelination (p < 0.001) in the brain, as well as infiltration of leukocytes (Th2 and Th27 cells) into the affected areas (p < 0.001). The acid suppressed EAE, even if treatment was started at the peak of the disease or in its chronic phase.

The number of new oligodendrocytes increased, while their precursors decreased, from which it can be concluded that ursolic acid stimulated the differentiation of these cells. Moreover, the therapy increased the number of myelinated neurons and repaired damaged axons and dendrites when treatment was started in the chronic phase of the disease.

In animals whose neuronal myelin was destroyed due to cuprizone, ursolic acid also caused the maturation of oligodendrocytes and repair of the membranes. In astrocytes treated with ursolic acid, the amount of ciliary neurotrophic factor (p < 0.01), which caused the maturation of oligodendrocytes, was increased by about three times compared to the control.

The effect of ursolic acid was mediated by PPARγ – when these receptors were blocked by antagonists or animals heterozygous for their gene were used, the drug ceased to be effective. The researchers also found that the CREB transcription factor is involved in triggering the release of the ciliary neurotrophic factor – when it was turned off, astrocytes did not produce the neurotrophic factor.

Ursolic acid is currently undergoing clinical trials in patients with tumors, and according to preliminary results, it is safe. It is known that this substance penetrates the blood-brain barrier and can act directly on the neurons of the central nervous system. Ursolic acid is a cheap, safe, and easy-to-administer drug that could potentially be used in the treatment of chronic multiple sclerosis, but this will require more validation and clinical trials in humans.

Drugs that can reverse the damage caused by multiple sclerosis do not yet exist, but their search has been going on for a long time. A few years ago, a possible target for such drugs was found – the expression of the b4 subunit of the G protein stimulates the differentiation of oligodendrocytes and the myelination of neurons.

Alisa Bakhareva

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Stem cells used against multiple sclerosis

Human fetal cells help attenuate the molecular and physiological signs of disease in patients with multiple sclerosis.

Mouse neural stem cell. (Photo: NIH Image Gallery / Flickr.com)

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The causes of multiple sclerosis are still not fully understood – although last year it was definitely established that it could be due to the Epstein-Barr virus. But we do know what happens in multiple sclerosis: the immune system attacks the myelin sheath of neurons. The myelin lipid sheath, which envelops the neural processes in several layers, is needed to ensure that neural impulses are transmitted quickly and to the correct address. Without it, the connection between the nerve centers in the brain, between the brain and muscles, between the brain and the sense organs, literally disappears; inflammation that develops during an immune attack destroys the neural processes themselves. Accordingly, in the treatment of multiple sclerosis, they try to somehow suppress the excessive activity of the immune system or somehow distract the immune system from the destruction of myelin on neurons.

But what to do with the damaged myelin sheath? It can be hoped that it will be restored by auxiliary cells of the nervous system – oligodendrocytes, which form the myelin winding on neurons. And you can add stem cells to help them. Such experiments have already been done with animals, and the results were encouraging: stem cells not only helped to restore the myelin sheath, but also protected myelin and neurons from immune attacks. In this case, we are not talking about stem cells in general, but about those that in the embryo give rise to the nervous system – both neurons and auxiliary cells, oligodendrocytes and some others, which are collectively called neuroglia. Embryonic stem cells in the process of embryonic development acquire a certain specialization, giving rise to certain organs; against multiple sclerosis, fetal progenitor cells of the nervous system should be used (based on pre-clinical results).

Employees of the Milan research institute IRCCS, together with colleagues from other scientific centers in Italy, moved from preclinical experiments to clinical ones. They injected germline stem cells into twelve patients aged 18 to 55 who had multiple sclerosis that lasted 2 to 20 years. The symptoms of all patients, even those who were diagnosed with multiple sclerosis only a few years ago, were very serious. Cells were taken from aborted embryos 10–12 weeks old; they were injected under the membranes of the spinal cord.

The results were just as encouraging as in animal experiments. An article in Nature Medicine states that after a few months, the cerebrospinal fluid of patients had a decrease in the number of inflammatory molecules that appear there in multiple sclerosis, and, conversely, an increase in the number of compounds that perform a neuroprotective function. In patients with multiple sclerosis, the volume of gray matter in the brain decreases – in those who received an injection of stem nerve cells, the volume of gray matter began to decrease more slowly, and it decreased more slowly, the higher the dose of stem cells was.