Oligodendrocyte

tissue destruction we term the primary injury. These mechanical forces predominately damage the central grey matter, due to its softer and highly vascularised nature, causing massive loss of essential cells, including local neurons, astrocytes, oligodendrocytes and endothelial cells in the vicinity of the injury site (Dumont et

A spinal cord injury does not occur in a single moment. Instead damage will continue to ensue for days to weeks after the initial injury. The initial impact and injury causes the immediate damage and death of oligodendrocytes and motor neurons. However, another wave of damage is caused by the secondary processes that occur after the injury. The spinal cord is a bundle of nervous tissue and neurons protected by the vertebral column that transmits electrical synapses, or messages, from the brain to

the endothelium of CNS capillaries forms a blood-brain barrier. endothelium of CNH capillaries forms a blood-brain barrier Extensive damage to oligodendrocytes in the CNS could result in loss of sensation and motor control. loss of the structural framework of the brain. inability to produce scar tissue at the site of an injury. decreased production of cerebrospinal fluid. a breakdown of the blood-brain

The term Glia is Greek in origin and means glue, this symbolic relationship between Glia’s name, and its function becomes ever more apparent when we learn that Glia cells secure the brain’s neurons together and protects them. Glial cells are crucial to the body’s ability to maintain homeostasis and contribute to almost all forms of homeostasis, such as regulating capillary flow, maintaining the blood brain barrier, extracellular respiration, and can even provide lactate to the neurons for energy

studies suggest a role for oligodendrocytes and brain demyelination in the pathophysiology of schizophrenia. To examine the putative role of oligodendrocytes in the pathophysiology of schizophrenia, animal studies are essential. Among possible animal models, the cuprizone (CPZ)-induced demyelination in C57BL/6 mice appear to be highly promising and deserving of close scrutiny. CPZ is a copper chelator and has been shown to specifically damage the myelin sheath and oligodendrocytes, but not to cause lesions

people with early MS. In order to determine whether recurring incidents of inflammatory SCD can significantly change the pattern of oligodendroglial repopulation and lead to demyelinated cortical lesions, the study compared NogoA+ and Olig2+ oligodendrocyte cells. The presence and activities of these cells in patients with early cases and mature stages of MS are examined and carefully analyzed. Results demonstrated a considerable decrease in the NogoA+ and Olig2+ cells for individuals with chronic

matter, which contains neuron cell bodies and white matter, which contains the nerve axons. Most of the nerve axons are concentrically wrapped around by lipid-rich biological membrane, known as the myelin sheath. In the CNS, myelin is produced by oligodendrocyte. a type of glial cell. (Pfeiffer et al., 1993). These electrical insulating, multilamellar membranes significantly increase the electrical resistance, in which to prevent leakage of electrical currents from the axons, as well as decrease electrical

the formation of lesions or plaques in the central nervous system – or CNS (Mayo Clinic Staff, 2014). Lesions are formed when oligodendrocytes – myelin-building cells – are lost causing the myelin sheath to thin or even completely breakdown leaving the nerve axon exposed and unable to send effective signals to your muscles (Huether and McCance, 2008). The oligodendrocytes attempt to remyelinate the axons but with multiple attacks, the

cell has an added function in which it is able to load a myelin peptide, extending the transfer from CD4+ to CD8+. This brings about a secondary autoimmunity as the CD8+ is able to respond to oligodendrocytes and cause them to lysis because the CD8+ is able to recognise myelin protein on these oligodendrocytes which constitute the myelin

in the inability to break down sulfatides in the lysosome of oligodendrocytes. The name is of greek origin, Leuko meaning white, dys meaning lack, and troph meaning growth. As a Leukodystrophy, the name implies that the disease is lacking growth in the white matter of the brain. The inability to break down sulfatides in the lysosomal complexes of the cell lead to the degeneration of the myelin sheath which are produced by oligodendrocytes. This disease is most commonly associated with the inability