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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 ...
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.
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 myelinoid or myelin organoid is a three dimensional in vitro cultured model derived from human pluripotent stem cells (hPSCs) that represents various brain regions, the spinal cord or the peripheral nervous system in early fetal human development.
The development of the nervous system in humans, or neural development, or neurodevelopment involves the studies of embryology, developmental biology, and neuroscience.These describe the cellular and molecular mechanisms by which the complex nervous system forms in humans, develops during prenatal development, and continues to develop postnatally.
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.
N-cadherin is expressed in regions of active remyelination and may play an important role in generating a local environment conducive to remyelination. [24] N-cadherin agonists have been identified and observed to stimulate neurite growth and cell migration, key aspects of promoting axon growth and remyelination after injury or disease. [25]