Search results
Results from the WOW.Com Content Network
While remyelination is very efficient in the early stages of multiple sclerosis, it causes remyelination to fail in the more chronic stages. [1] As axons are left bare, without myelin, their conduction velocity goes down due to a lack in increased potential between the Nodes of Ranvier. Not only does conduction go down, but a naked axon is also ...
In addition, the interaction between transplanted cells and immune cells and the effect of inflammatory immune cells on remyelination have yet to be fully characterized. If the failure of endogenous remyelination is due to an unfavorable differentiation environment, then this will have to be addressed prior to transplantation.
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.
This is why symptoms can vary greatly between different individuals, depending on where their lesions occur. Repair processes, called remyelination, also play an important role in MS. Remyelination is one of the reasons why, especially in early phases of the disease, symptoms tend to decrease or disappear temporarily.
A single oligodendrocyte can extend its processes to cover up to 40 axons, that can include multiple adjacent axons. [2] The myelin sheath is not continuous but is segmented along the axon's length at gaps known as the nodes of Ranvier. In the peripheral nervous system the myelination of axons is carried out by Schwann cells. [1]
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.
Neuroregeneration differs between the peripheral nervous system (PNS) and the central nervous system (CNS) by the functional mechanisms involved, especially in the extent and speed of repair. When an axon is damaged, the distal segment undergoes Wallerian degeneration, losing its myelin sheath.
This 'jumping' continues until the action potential reaches the axon terminal. [3] [4] [5] Once there, the electrical signal provokes the release of chemical neurotransmitters across the synapse, which bind to receptors on the post-synaptic cell (e.g. another neuron, myocyte or secretory cell).