Oligodendrocytes in Disease
A plethora of central nervous system diseases cause damage to oligodendrocytes resulting in demyelination and leading to neurological disability through the resulting loss of conduction speed. Myelin diseases can be categorized into two broad types: those that cause targeted chronic damage to oligodendrocytes specifically, such as in multiple sclerosis, and those in which the oligodendocyte is injured as a result of non-specific disease or damage, as is the case in ischemia or trauma.
In either case, normal conduction is no longer possible via the affected pathways resulting in plastic change of the chronically demylinated axon. Normally clustered at the nodes of Ranvier, sodium channels are redistributed more evenly across the axon. This redistribution has important functional consequences: conduction across the axon is re-established, but the speed of conduction is reduced. Normal conduction speed can be restored with remyelination.
Spontaneous remyelination has been observed in the human central nervous system, though remyelinated axons display myelin that is disproportionately small compared to the normal myelin on an axon of similar diameter. Functionally, conduction speed, and therefore neurological function, is fully restored by remyelination, though it should be noted that the restoration of conduction velocity occurs before full remyelination.
Read more about this topic: Oligodendrocyte Progenitor
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