Myelin
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 the act of demyelinating, or the loss of the myelin sheath insulating the nerves, and is the hallmark of some
neurodegenerative autoimmune diseases.
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 (Vlassara, et. al. 1985)(Thornally 2002). 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.
*
Multiple sclerosis, caused by loss of myelin
*
The Myelin Project*
Athabasca University Biological Psychology Website*
The MS Information Sourcebook, Myelin*
The Myelin Repair Foundation*
H & E Histology*
Luxol Fast Blue: Modified Kluver's Method to stain for Myelin Sheath* Vlassara H, Brownlee M, Cerami A.
Recognition and uptake of human diabetic peripheral nerve myelin by macrophages. Diabetes. 1985 Jun;34(6):553-7.
PMID: 4007282 * Thornalley PJ.
Glycation in diabetic neuropathy: characteristics, consequences, causes, and therapeutic options. Int Rev Neurobiol. 2002;50:37-57.
PMID: 12198817 
