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Myelin is an electrically-insulating phospholipid layer that surrounds the axons of many neurons. It is an outgrowth of glial cells: Schwann cells supply the myelin for peripheral neurons, whereas oligodendrocytes supply it to those of the central nervous system. Myelin is considered a defining characteristic of the (gnathostome) vertebrates, but it has also arisen by parallel evolution in some invertebrates. Myelin was discovered in 1878 by Louis-Antoine Ranvier.
Additional recommended knowledge
Composition of myelin
Myelin made by different cell types varies in chemical composition and configuration, but performs the same insulating function. Myelinated axons are white in appearance, hence the "white matter" of the brain.
Myelin is composed of about 80% lipid fat and about 20% protein. Some of the proteins that make up myelin are Myelin basic protein (MBP), Myelin oligodendrocyte glycoprotein (MOG), and Proteolipid protein (PLP). Myelin is made up primarily of a glycolipid called galactocerebroside. The intertwining of the hydrocarbon chains of sphingomyelin serve to strengthen the myelin sheath.
Function of myelin layer
Demyelination and Dysmyelination
Demyelination is the act of demyelinating, or the loss of the myelin sheath insulating the nerves, and is the hallmark of some neurodegenerative autoimmune diseases, including multiple sclerosis, transverse myelitis, chronic inflammatory demyelinating polyneuropathy, Guillain-Barre Syndrome. Sufferers of Pernicious Anaemia can also suffer nerve damage if the condition is not diagnosed quickly. Sub-Acute Combined Degeneration of the Cord Secondary to Pernicious Anaemia can lead to anything from slight peripheral nerve damage to severe damage to the central nervous system affecting speech, balance and cognitive awareness. When myelin degrades, conduction of signals along the nerve can be impaired or lost, and the nerve eventually withers.
The immune system may play a role in demyelination associated with such diseases, including inflammation causing demyelination by overproduction of cytokines via upregulation of tumor necrosis factor (TNF) or interferon.
Research to repair damaged myelin sheaths is ongoing. Techniques include surgically implanting oligodendrocyte precursor cells in the central nervous system and inducing myelin repair with certain antibodies. While there have been some encouraging results in mice (via stem cell implant), it is still unknown whether this technique can be effective in humans.
Dysmyelination on the other hand is different from the lesions producing process of active demyelination and is characterized by defective structure and function of myelin sheaths. Such defective sheaths often arise from genetic mutations affecting the biosynthesis and formation of myelin. Examples of human diseases where dysmyelination has been implicated include leukodystrophies (Pelizaeus-Merzbacher disease, Canavan disease, Phenylketonuria) and schizophrenia.   
Symptoms of Demyelination
Demyelination destruction or loss of the myelin sheath typically results in diverse symptoms. The symptoms are determined by the functions normally contributed by the affected neurons.
Damage to the myelin sheath disrupts signals between the brain and other parts of the body producing a range of symptoms. Symptoms are often heterogeneous — dependent on pathophysiology of demyelination — differing from patient to patient, and have different presentations upon clinical observation and in laboratory studies.
|This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Myelin". A list of authors is available in Wikipedia.|