In neuroscience, 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 while oligodendrocytes supply it to those of the central nervous system. The myelin produced by the different cell types varies in its chemical composition or configuration, but performs the same function. Myelinated neurons 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 sphingolipid called sphingomyelin, and it is thought that the intertwining of the hydrocarbon chains of sphingomyelin serve to strengthen the myelin sheath.

The main consequence of a myelin layer (or sheath) is an increase in the speed at which impulses propagate along the myelinated fiber. Along unmyelinated fibers, impulses move continuously as waves, but, in myelinated fibers, they hop (or "propagate by saltation"). Myelin increases resistance by a factor of 5,000 and decreases capacitance by a factor of 50. Myelination also helps prevent the electrical current from leaving the axon and causing a short-circuit in the brain. When a peripheral fiber is severed, the myelin sheath provides a track along which regrowth can occur. Unmyelinated fibers and myelinated axons of the mammalian central nervous system do not regenerate.

Demyelination is a loss of myelin and is the root cause of symptoms experienced by patients with diseases such as multiple sclerosis and transverse myelitis. The immune system may play a role in demyelination associated with such diseases. Heavy metal poisoning may also lead to demyelination. When an axon's myelin degrades due to these diseases, conduction can be impaired or lost.

Research is currently being undertaken to repair damaged myelin sheaths. These 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, it is still unknown whether this research will provide a cure for demyelination-related diseases.

Other research implicates exogenous and endogenous glycations and Advanced Glycation Endproducts are important in the age-related destruction of myelin, particularly in peripheral neuropathy. It is reasonable to suspect that all nerves, especially high activity nerves such as the sensory nerves in the eye and ear, are similarly affected. Until effective therapies are developed, dietary restriction of exogenous AGEs and strongly glycation forming sugars, such as fructose and galactose, is the best available approach.

Adrenoleukodystrophy (ALD) is a disease that is found in young boys at around age six. This is a degenerative disease that strips myelin off of the nerves. Carriers may become blind, unable to move, and lose control of many other functions. Myelin is important in the function of these abilities.


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