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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 ]
Myelin is formed by oligodendrocytes in the central nervous system and Schwann cells in the peripheral nervous system.Therefore, the first stage of myelinogenesis is often defined as the differentiation of oligodendrocyte progenitor cells (OPCs) or Schwann cell progenitors into their mature counterparts, [4] followed by myelin formation around axons.
Repeated attacks lead to successively fewer effective remyelinations, until a scar-like plaque is built up around the damaged axons. These scars are the so-called "scleroses" that define the condition. They are named glial scars because they are produced by glial cells, mainly astrocytes, and their presence prevents remyelination. Therefore ...
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.
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.
In chronic MS lesions where remyelination is incomplete, there is evidence that there are oligodendrocytes with processes extending toward demyelinated axons, but they do not seem to be able to generate new myelin. [63] The mechanisms that regulate differentiation of OPCs into myelinating oligodendrocytes are an active area of research.
Human axon growth rates can reach 2 mm/day in small nerves and 5 mm/day in large nerves. [4] The distal segment, however, experiences Wallerian degeneration within hours of the injury; the axons and myelin degenerate, but the endoneurium remains. In the later stages of regeneration the remaining endoneurial tube directs axon growth back to the ...
A repair process, called remyelination, takes place in the early phases of the disease, but the oligodendrocytes are unable to completely rebuild the cell's myelin sheath. [90] Repeated attacks lead to successively less effective remyelinations, until a scar-like plaque is built up around the damaged axons. [90]