Essay On Oligodendrocytes

Multiple sclerosis (MS) involves an autoimmune process that develops when a previous viral insult to the nervous system has occurred in a genetically susceptible individual. B lymphocytes, plasma cells, and activated T cells, along with proinflammatory cytokines, cause inflammation, oligodendrocyte injury and demyelination. Early inflammation and demyelination lead to irreversible axonal

Multiple Sclerosis is an unpredictable, potentially disabling disease of the central nervous system that can affect the brain, spinal cord, and nerves. Multiple Sclerosis can range from relatively benign to disabling to devastating. The disease is considered an autoimmune disease in which the body’s immune system attacks its own tissues causing damage to the myelin sheath, which covers the nerve fibers, and causes communication problems between the brain and the rest of the body and ultimately cause the nerves to deteriorate or become permanently damaged. When any part of the myelin sheath is damaged or destroyed the nerve impulses that travel back and forth to the brain and spinal cord are interrupted, this produces a range of different symptoms.

Multiple sclerosis (MS) is an unpredictable, immune mediated disease of the central nervous system (CNS) (Definition of MS). This disease is estimated to affect more than 400,000 people in the United States alone, and about 2.5 million worldwide. In the United States, about 200 new cases of MS are discovered weekly (Pietrangelo, Anne and Higuera, Valencia) . In a healthy person, an insulation covering called myelin, coats the nerve fibers in the CNS (Article from mom). When one develops MS, the communication between their brain and other parts of his/her body is disrupted as “an abnormal immune-mediated response” attacks the myelin coating that encloses nerve fibers in the CNS. This causes a disturbance in communication between the CNS and

Multiple Sclerosis (MS) is a neurologic disease that affects the Central Nervous System (CNS) through cellular immune response and the demyelination of CNS white matter (McCance et al., 2014, pp. 630–633). The initial causes of MS are unknown however, it is believed that it could possibly be due to an immune response to an initiating infection or an autoimmune response to CNS antigens on the myelin itself (Brück, 2005) (Miljković and Spasojević, 2013). MS is a result of the degradation of the myelin sheath surrounding neurons and therefore disrupts the transmission of action potentials along these cells. MS can display itself in the form of symptoms ranging from muscle weakness to trouble with sensation and coordination (NHS, 2016). The degradation of myelin leads the body to attempt to remyelinate the neurons, a process that in turn leads to the thickening of the cell by glial cells and this causes lesions to form (Chari, 2007). It is this thickening (sclerae) from which the disease gets its name. Sufferers of MS can either have a relapsing type of MS, in which there are episodes that lead to the worsening of symptoms for a period of time, or a progressive type of MS where symptoms gradually progress and worsen (McCance et al., 2014, pp. 630–633).

The breakdown of the myelin sheath is caused from a mutation of the gene that makes the Adrenoleukodystrophy protein (ALDP). This ALD protein helps the body metabolize saturated very-long-chain fatty acids found in the serum and tissues of the central nervous system. The newly mutated gene no longer acts as a help aid to breaking down the long-chain fats. Therefore, the body starts accumulating an abnormal amount of fat in the nervous system, adrenal gland and testes that sets off an unusual response in the immune system; demyelination.

Myelin, the common factor in each disease, is a subsatnce that surrounds and insulates axons on some nerve cells, allowing for a faster transporting of signals and proper functioning of the nervous system. A demyelinating disease results in the damage of nerve fibers in the brain and spinal cord due to the myelin sheath being destroyed, which is life threatening.

“Multiple sclerosis (MS) is a disease in which your immune system attacks the protective sheath (myelin) that covers your nerves” (Mayo Clinic). The immune system is a defensive system that protects your body from diseases and illnesses such as parasites and bacteria (Science Museum). Not only does your immune system defend the human body but also the immune system can work against the body, which is known as autoimmune disease. Since the immune system is working against your body to attack the myelin, this creates an opportunity for multiple sclerosis to invade the nerves in the central nervous system (CNS). The myelin within the body acts like insulation to protect and coat the nervous system (National Multiple Sclerosis Society). Once the myelin is eroded, the nerves become exposed which then causes signals to and from the brain to become distorted or irrupted causing a wide range of symptoms to occur (National Multiple Sclerosis Society). The effect of the myelin eroding is an irreversible process (Mayo Clinic). “The damaged myelin forms scar tissue (sclerosis), which

2010). The neuroinflammation is an early, non-specific immune reaction to tissue damage or pathogen invasion (Lee et al. 2010). Inflammation of the central nervous system (CNS) is characterized by increased glial activation, pro-inflammatory cytokine concentration, blood-brain-barrier permeability, and leukocyte invasion (Lee et al. 2010). Microglia are cells that support and protect neuronal functions (Lee at al. 2010). They act as the first and main form of active immune defense that orchestrate the endogenous immune response of the Central Nervous System. The microglia play a central role in the cellular response to pathological lesions such as Aβ. Aβ can attract and activate microglia, leading to clustering of microglia around Aβ deposits sites in the brain (Lee et al. 2010). Even though microglia have neuroprotective functions, neurotoxic mechanisms which involves continuous activation of microglia and toxic factors are released by microglia, which may lead to neuroinflammation (Lee et al. 2010). Astrocytes (star-shaped glial cells) are the most abundant cells in the brain and are located in the brain and spinal. Astrocytes have various functions such as: biochemical support of endothelial cells of the BBB, supplying nutrients to the nervous tissue, maintenance of extracellular ion balance, and healing the brain and spinal cord following traumatic injury (Lee et al., 2010). Chemokines are released by astrocytes which attract microglia and they further express proinflammatory products, thus increasing neuronal damage in the pathogenesis of AD (Lee et al., 2010). Astrocytes play a critical role in Aß clearance and degradation, and they also provide trophic support to neurons forming a protective barrier between Aß deposits and neurons (Wyss-Coray et al., 2003). Neurons contribute to the production of

Multiple sclerosis, or MS as it is more commonly referred, is an immune mediated disease that involves the body's own defense mechanism, specialized immune cells, that ultimately attacks the central nervous system. Specifically, the myelin protein that coats axons and forms an electrically insulating layer for quicker processing of the nervous system, is attacked by cytotoxic cells that have crossed into the CNS. In a healthy patient, the blood brain barrier cannot be crossed by cytotoxic cells and it is speculated that an environmental component or outside source mediates this crossing. When the myelin is attacked, it forms scars in the CNS, as multiple sclerosis literally translates to “many scars,” which is the direct result of the disease. The scars disrupt the normal nerve impulses that travel through the central nervous system, and can cause a variety of symptoms including loss of cognition, fatigue, or numbness in the body (Evidence).

All of the activated T-cells then release cytokines and adhesion molecules that enable the T-cells to adhere to and cross over the blood-brain barrier, which normally prohibits the flow of substances into the brain (8,9). The proteins in these T-cells bind to myelin fragments on microglial cells and undergo a secondary activation (10), after which they multiply and release more cytokines, further invading the nervous system (11) and inflaming and damaging the blood-brain barrier. The greatly weakened barrier becomes easily permeable, allowing additional immune system cells, such as B-cells and cytotoxic T-cells to cross over (12). Once through the barrier, B-cells produce antibodies which bind to the oligodendracytes (the cells of the CNS which create myelin) and the myelin itself. Associated macrophages procede to destroy the myelin and may also damage the oligodendracytes (13).

Inflammation is a reaction of tissues in response to any injury the human or vertebrae sustains. Neuroinflammation is the inflammatory response by the glial cells that are present in the nervous system along with neurons. It is an immune response to pathogen invasion or tissue damage most likely to be caused by Infectious bacteria, Traumatic brain injury (TBI), or toxic metabolites. The nervous system contains neurons and glial cells composed of astrocytes, microglia, oligodendrocytes, ependymal cells in the Central nervous system (CNS), and Schwann cells, satellite cells in Peripheral nervous system (PNS). The glial cells are non-neuronal cells that help to form myelin, maintain homeostasis, provide support for neurons with nutrients, destroy

A cohort of mice underwent a second mTBI after 24 hours. Mice from both WT and Tg groups were assessed 2 days, 9 weeks, and 16 weeks after mTBI treatment. Primarily, H&E stain was employed along with Gomori’s iron stain to localize site and severity of mTBI injury. The degree of A deposition in the somatosensory cortex (SSC), the perihippocampal cortex (PHC), and the hippocampus (HP) of both hemispheres was determined by 4G8 immunostaining. In addition, GFAP staining was used to quantify the population of astrocytes at the site of the injury. Furthermore, Sandwich ELISA was utilized in mice groups 16 weeks after injury to measure A40 and A42 peptide levels in various brain regions, including the cerebral cortex, the hippocampus, and the cerebellum. Such tissues were also analyzed for isoprostane levels that are produced by lipid peroxidation. Isoprostanes were also detected in urine samples at various survival periods. Moreover, mice underwent Morison water maze (MWM) and composite neuroscore (NS) tests at 16 weeks’ post-injury to examine cognitive and motor functions respectively. Uryu and collegues found a significant increase in iron deposits and reactive astrocytes in the repetitive mTBI postmortem sections of Tg mice, when compared to other groups at 16 weeks after the injury. This was not the case in WT mice. Similarly, there was a significant increase in the A burden within select brain regions (i.e. SSC, PHC, HP) of single and

Multiple sclerosis (MS) is a demyelinating disease which affects nerves in the brain and spinal cord which results problems in muscle movement, balance and vision. The nerve fiber in the brain and spinal cord are surrounded by layer of protein called myelin which help to protects the nerve and helps electrical signals from the brain travel to the rest of the body. In case of multiple sclerosis the tissue which is affected is myelin sheaths. During multiple sclerosis something goes wrong with immune system and immune system starts attacking myelin sheaths as they recognize them as foreigner bodies. During macrophage myelin sheaths is engulf and they are presented as foreign bodies to the T-lymphocytes cell which produce antibodies and destroy

Glial cells are the most numerous cells in the brain, outnumbering neurons nearly 3:1, although smaller and some lacking axonal and dendritic projections. Once thought to play a subpar role to neurons, glial cells are now recognized as responsible for much greater functions. There are many types of glial cells, including: oligodendrocytes, microglia, and astrocytes. Oligodendrocytes form the myelin sheath in the CNS, by wrapping themselves around the axons of neurons. Their PNS counterpart, Schwann cells, are also considered glial cells. This sheath insulates the axon and increases the speed of transmission, analogous to the coating on electrical wires. Microglia are considered to be “immune system-like”; removing viruses, fungi, and other wastes that are present. Astrocytes, however, are considered to be the most prominent. Their functions span throughout the brain, including, but not limited to: the synchronization of axonal transmission via G-protein-coupled receptors, blood flow regulation via the dilation of blood vessels, and the performance of reactive gliosis in conjunction with microglia. Both astrocytes and oligodendrocytes develop from neuroepithelial cells. Other types of glial cells include Radial glia, which direct immature neuron migration during development.

In the last two decades increasing research has been focused on the role of astrocytes in brain physiology and pathology: astrocytes were shown to be actively involved in neuronal communication and homeostasis. The contribution of inflammation in epilepsy and epileptogenesis has pointed to astrocytes as key components of this condition characterized by hyperexcitability of the neural tissue. In fact, astrocytes represent an important source of immunologically relevant cytokines and chemokines which have been demonstrated to increase neuronal excitability in different experimental models. As almost 30% of epileptic patients are pharmacoresistant, understanding the role of astrocytes in the pathology could provide new targets for the development