ll Formalin- prepared optic nerves (ON) was mainly used as the materials and sources of information in the study. To identify the human ON areas where demyelination has occurred, Jennings and Caroll used luxol fast blue (LFB) and hamatoxylin and eosin. Cat ON, on the other hand, were stained with toluidine to distinguish the myelin sheaths in preparation for electron microscopy processing. After this, immunohistochemistry was effectually conducted in order to differentially mark the neuroglia. The digital images formed were then examined and evaluated to quantify the data. Results revealed the presence of oligodendroglial cells in MSON lesions, which further confirms the link between remyelination as a result or consequence of …show more content…
Subpial cortical demyelination (SCD) has been recently found to manifest among 90% of progressive MS patients and is even present to 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 MS, but those in the early stages of MS showed a different result. Moreover, during the demyelination phase, repeated stimulation of SCD in the experimental rats stemmed to a transitory loss of NogoA+ but did not have a similar effect on the Olig2+ cells. This was followed by the complete repopulation and remyelination of the oligodendroglial cells, notwithstanding the four preceding periods of demyelination. These results indicate successful remyelination in subpial cortical lesions among the rats even after repeated SCD, an indication only apparent to early MS but not to chronic cases. Furthermore, the data obtained demonstrated that the four cycles of continuous demyelination and remyelination process did not effectively sustain an independent remyelination that has been observed in chronic MS lesions. The results of the
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 (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).
It is suggested by previous studies that the damage of the myelin sheath in MS involves the activation of inflammatory factors including the CD4+ T cells, CD8+ T cells, B cells, macrophages and microglia cells (Luccinetti et al., 1996; Lassmannet al., 2012). However, whether the immune response triggers the onset of MS, or is a consequence of the disease process is currently not clear. Interestingly, several recent studies suggested that the prevalence rate of MS is significantly increased with latitude, which implies that not only the geographical (environmental) differences but racial and ethnic differences may play a role in the worldwide MS distribution (Rosati, 2001; Simpson et al., 2011).
Multiple sclerosis, or MS, is a disease of the central nervous system. The central nervous system is made up of the brain and spinal cord. Both have nerve fibers that are wrapped in a myelin sheath. In MS, the myelin sheath becomes inflamed and gradually is destroyed. With the destruction of the myelin sheath comes an array of symptoms that may include numbness or tingling, balance problems, weakness, muscle spasms, and blurred vision.
Multiple sclerosis, or MS, is a disease of the central nervous system. The central nervous system is made up of the brain and spinal cord. Both have nerve fibers that are wrapped in a myelin sheath. In MS, the myelin sheath becomes inflamed and gradually is destroyed. With the destruction of the myelin sheath comes an array of symptoms that may include numbness or tingling, balance problems, weakness, muscle spasms, and blurred vision.
“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
Multiple sclerosis, or MS, is an autoimmune disease in which the body’s immune system targets the central nervous system (National Multiple Sclerosis Society, 2016). The central nervous system is mainly made up by the brain, nerves, spinal cord, and optic nerves (National Multiple Sclerosis Society, 2016). The main target in MS is myelin, the substance that protects the nerve fibers within the central nervous system (National Multiple Sclerosis Society, 2016).
Multiple Sclerosis is an inflammatory demyelinating neurodegenerative disorder of the central nervous system that has the potential to cause significant disability in those affected through the body's immune system attacking and destroying the myelin sheaths surrounding the axons. Myelin is rich in lipids and proteins that form layers around the nerve fibers and acts as insulation and protection. This damage to the myelin in the CNS, and to the actual nerve fibers, has the potential to block the transmission of nerve signals between the brain and spinal cord and also other parts of the body. This disruption of the nerve signals produces the primary symptoms of MS which then possibly lead to secondary and tertiary symptoms stemming from these
Multiple sclerosis is a disease of the central nervous system. It most commonly occurs in individuals between the ages of twenty and forty (1) and in higher numbers of women than men (2). In Multiple Sclerosis (or "MS") a loss of the nerves' axon coating myelin prohibits the nerve axons from efficiently conducting action and synaptic potentials. Scar tissue (called plaques or lesions) forms at the points where demyelination occurs in the brain and spinal cord, hence the name "Multiple Sclerosis"or "many scars" (3). The demyelination found in MS is thought to be caused by an autoimmune process, in which the body's immune system attacks its own healthy tissue (4). Other diseases thought to have an autoimmune basis are
Multiple sclerosis, commonly known as MS, is an auto-immune disease. An auto-immune disease is one in which the body attacks itself. In this particular disease, the central nervous system is being attacked. Specifically, the myelin sheath, or the fatty substance that coats and protects nerve fibers in the brain and spinal cord, is attacked. The attacks cause scar tissue, which makes it difficult for signals to travel between the brain and body. Eventually, the nerves may deteriorate, which is a process that is completely irreversible [5]. See the figure below for more detail.
Multiple Sclerosis, also known as “MS” is a chronic condition where the immune system begins to destroy the myelin sheath that covers the nerves in the body and affects the brain and spinal cord (Mayo Clinic Staff, 2014). The myelin sheath is used for protection of the nerves in which these nerves aid to transport nerve impulses all over the body (Ruto, 2013). Once the body’s immune system attacks the myelin sheath, it begins to disintegrate which affects the conductivity of the nerve impulse and impedes the message transmission from the brain to the rest of the body (Ruto, 2013). In turn, the impulses are changed which results in problems in the muscle such as weakness, imbalance and spasms and the body could end up
Multiple sclerosis (MS) is a potentially disabling disease of the brain and spinal cord, particularly the central nervous system (CNS). In MS the immune system attacks the myelin, which is the protective sheath that covers the nerve fibers and causes communication between your brain and the rest of your body. Eventually, the disease can cause the nerves to deteriorate or even lead to permanent damage. They deteriorate in variable degrees and produce significant disability within 20-25 years in more than 30% of patients, (Luzzio, 2016). The majority of people diagnosed with MS are adults between the ages of 20 and 45; twice as many women are affected compared to men. However, MS can present itself in childhood or late middle age, but is uncommon. According to Goldenberg (2012), there is no known cause for this debilitating disease, but it appears to involve a combination of genetic susceptibility and a nongenetic trigger, such as a virus, metabolism, or environmental factors
There are four different patterns of inflammation in the white matter that is associated with individuals with multiple sclerosis (Lassmann et. al. 2007).The first pattern of inflammation is associated with the demyelination caused by macrophage activity. This pattern of inflammation is characterized by perivascular demyelination with radial expansion and extensive remyelination. The second pattern of inflammation demyelination is associated with antibody and complement activity. The lesions exhibited in this pattern are similar to lesions that occur in the first pattern except that the active demyelination sites demonstrate additional deposition of immunoglobulin (Ig) and activated complement in pattern 2. Immunoglobulins are antibodies that
The Experimental autoimmune encephalomyelitis (EAE) is the most commonly used model for Multiple Sclerosis. The Multiple Sclerosis is a chronic inflammatory, neurodegenerative disease, which is predominantly in young adults from ages 20-40 years. The immune response for this inflammation is demyelination, axonal transection and eventually leading to cognitive deficits 4. The EAE was induced to the mice via subcutaneous injection of 200 µg of auto-antigen myelin oligodendrocyte glycoprotein (MOG) peptide 4. Then, the mice were tested for spatial learning and memory tasks through the use of Barnes Maze method for both the control and EAE induced mice. This method is a hippocampal behavioral task, where the mice must learn the spatial location of a target hole to escape from the visual and auditory stimuli 4. After obtaining the brain tissue samples from the mice, they were stained using Nissl Stain and later sectioned to evaluate branching and spine count of the hippocampal CA1
Malik, O., Donnelly, A., & Barnett, M. (2014). Fast facts: Multiple sclerosis (3rd ed.). [Proquest Ebook Central]. Retrieved from http://www.ebookcentral.proquest.com