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Remyelination is the process of propagating oligodendrocyte precursor cells to form oligodendrocytes to create new myelin sheaths on demyelinated axons in the Central nervous system (CNS). This is a process naturally regulated in the body and tends to be very efficient in a healthy CNS. [ 1 ]
The process and mechanistic function of myelinogenesis has traditionally been studied using ultrastructure and biochemical techniques in rat optic nerves. The implementation of this method of study has long allowed for experimental observation of myelinogenesis in a model organism nerve that consists entirely of unmyelinated axons. Furthermore ...
Neurodevelopment in the adult nervous system includes mechanisms such as remyelination, generation of new neurons, glia, axons, myelin or synapses. Neuroregeneration differs between the peripheral nervous system (PNS) and the central nervous system (CNS) by the functional mechanisms and especially, the extent and speed.
A repair process, called remyelination, takes place in early phases of the disease, but the oligodendrocytes are unable to completely rebuild the cell's myelin sheath. Repeated attacks lead to successively less effective remyelinations, until a scar-like plaque is built up around the damaged axons.
The process of generating myelin is called myelination or myelinogenesis. In the CNS, oligodendrocyte progenitor cells (OPCs) differentiate into mature oligodendrocytes, which form myelin. In humans, myelination begins early in the 3rd trimester, [ 11 ] although only little myelin is present in either the CNS or the PNS at the time of birth.
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Each process reaches out to an axon and spirals around it, creating a myelin sheath. The myelin sheath insulates the nerve fiber from the extracellular fluid and speeds up signal conduction along the nerve fiber. [34] In the peripheral nervous system, Schwann cells are responsible for myelin production.
These markers are specific for the different processes that drive the formation of plaques: inflammation, myelin breakdown, astrogliosis, oligodendrocyte injury, neurodegeneration, axonal loss and remyelination. MS lesions evolve differently during early versus chronic disease phases, and within each phase, different kind of activity appears.