Search results
Results from the WOW.Com Content Network
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 ]
Oligodendrocyte progenitor cells (OPCs), also known as oligodendrocyte precursor cells, NG2-glia, O2A cells, or polydendrocytes, are a subtype of glia in the central nervous system named for their essential role as precursors to oligodendrocytes and myelin. [1] They are typically identified in the human by co-expression of PDGFRA and CSPG4.
Immature oligodendrocyte: Sometimes referred to as premyelinating oligodendrocytes, these cells extend "pioneer processes" which contact axons and anchor premyelinating oligodendrocytes to neurons such that they are poised to commence myelinogenesis in response to axonal signals. These pioneer processes grow longitudinally along their target axons.
In this latest study, the researchers used a toxin from the venom of a green mamba snake to identify and locate a receptor protein, M1R, on oligodendrocyte precursor cells (OPCs), which fail to ...
Oligodendrocytes are a type of glial cell, non-neuronal cells in the central nervous system.They arise during development from oligodendrocyte precursor cells (OPCs), [8] which can be identified by their expression of a number of antigens, including the ganglioside GD3, [9] [10] [11] the NG2 chondroitin sulfate proteoglycan, and the platelet-derived growth factor-alpha receptor subunit (PDGF ...
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.
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.
Increasing oligodendrocyte cholinergic stimulation, AChEIs, and other cholinergic treatments, such as nicotine, possibly could promote myelination during development and myelin repair in older age. [38] Glycogen synthase kinase 3β inhibitors such as lithium chloride have been found to promote myelination in mice with damaged facial nerves. [39]