Neurological Disorders: The Paractin Effect

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).

Multiple sclerosis (MS) is an acquired demyelinating disease of the central nervous system (CNS) that typically is diagnosed in the second or third decade of life. Normally, nerves are enclosed in myelin sheaths that help facilitate transmission of nerve impulses within the CNS and the peripheral nervous system throughout the body. In patients with MS, the myelin sheath is damaged and eventually degenerates, causing patches of scar tissue called plaques or lesions to occur anywhere randomly on the myelin sheath (Ruto, 2013). This results in impaired nerve conductivity, which interferes with message transmission between the brain and the other parts of the body. As a result, impulse transmission is altered, distorted, short-circuited,

Multiple sclerosis is an unpredictable, crippling neurological disease of the central nervous system, which affects the flow of information within the brain, and between the brain and body. The name is this disease refers to multiple areas of scarring throughout the brain and spinal cord. This scarring is a result of what happens when the body attacks itself. A substance called Myelin surrounds the nerves to help protect them (Healthline.com, 2015). Multiple Sclerosis is thought to occur in a genetically susceptible individual (although there is no evidence to show that the disease is directly inherited) influenced one or more environmental factors. MS is thought to be an autoimmune disease, however others disagree as the target of the immune

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).

MS is an autoimmune disease, meaning the immune system attacks the bodys own myelin sheath protection. The damaged myelin and axon fibers is caused by overactivated T cells.

Multiple sclerosis, also known as MS, is an autoimmune and inflammatory disease that is very painful for both the patient and care giver. In the disease, there is inflammation and neurodegeneration acting at the same time. There is currently no known primary cause of multiple sclerosis. The disease is however characterized by damaged fatty myelin sheaths around the axons of the brain and the spinal cord. Myelin is a mixture of proteins and phospholipids that protects many nerve fibers enabling speed at which impulses are conducted. It is pathologically characterized as the presence of glial scars all over in the central nervous system. The disease was discovered by the French neurologist Jean-Martin Charcot in 1868 when he examined the brain

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

Multiple Sclerosis is a disease that can impact many different parts of the body. It starts out by the immune system attacking the myelin that surrounds the nerve fibers in the Central Nervous System. Once the myelin tissue is damaged, it forms a type of scar tissue that essentially causes the sclerosis. It then sends nerve impulses back and forth between the brain and spinal cord that can cause many different ranges of symptoms. Scientists are still researching the cause for this disease; however, there have been great advancements since it was first discovered back in the eighteen-hundreds. From conducting research over the years, scientists have been able to collect data that gives a further insight into how MS works. There is no cure

The exact cause of MS is unknown. However, its pathogenesis is associated with irregular immune responses against CNS antigens, interference of the blood-brain barrier (BBB) and trans endothelial migration of activated leukocytes, as well as chemokines and cytokines, from peripheral circulation to the CNS. In active disease, there appears to be ongoing inflammatory as well as neurodegenerative processes within the CNS atmosphere. The triggering event for the first attack of MS remains projected. It is assumed that genetic and environmental factors are involved in the progress of MS. (Borazanci, 2009, p. 2)

sheath is made up of protein and fatty substances. It insulates our nerve fibers both in

human MS. In this model, the injection of BM-MSCs improvedthe clinical course and promoted peripheral T cell tolerance tomyelin proteins, thus reducing the migration of pathogenic T cellsto the CNS (Morando et al., 2012; Bai et al., 2009; Gerdoni et al.,2007; Zhang et al., 2005). In this model setting, the therapeuticeffects of MSCs were not likely attributable to graft- or host-driven remyelination, but rather were mediated by an immunemodulatory mechanism guarding the CNS from immune-mediatedinsult (Morando et al., 2012; Rafei et al., 2009). Similarly, BM-MSCs have been reported to have been successfully used in animalmodels of acute disorders, such as stroke or spinal cord injury,while they are disappointingly unable to remedy the neurologicaldeficits when chronic neural damage occurs. These observationssuggest that the immunosuppressive nature of BM-MSCs, whichis substantially increased by inflammatory cues, allows them tomodulate immune response and inhibit inflammation (Uccelli et al.,2011).These findings pose the question of whether the reported ben-eficial effects of BM-MSCs in immune models such as EAE are dueto suppression of the peripheral immune response that damagesmyelin or due to immune-independent mechanisms of action, suchas the direct replacement of the dying cells, oligo/neuroprotection,and/or enhancing endogenous repair. This question is furtherhighlighted by a recent study conducted in a non-immune toxinmodel in which intravenously injected BM-MSCs did

Specifically, several metabolites warrant further discussions. In mouse liver samples, N-acetylgalactosamine 4-sulphate, also known as GalNAc4S, increased by 2.17 fold compared with normal controls (p<0.05). N-acetylgalactosamine 4-sulphate is key component of glycosaminoglycans (GAG) including dermatan, keratan and chondroitin sulfate), and is found in elevated concentrations in the urine of MPS patients. More interestingly, since Hex enzyme may also cleave GAG, mice and cats with SD showed GAG accumulation and MPS-like phenotype [14,15]. The increase in N-acetylgalactosamine 4-sulphate may be a side effect of Hex enzyme deficiency. Significant higher total GAG levels in liver of SD mice compared with normal mice (20.7±2.6 vs 8.4±1.1µg GAG/mg protein) were also observed (Figure 2). Therefore, GAG can be used as a novel biomarker of SD. N-Acetyl-L-aspartic acid, downregulated in hippocampus of SD patients, is a neuronal osmolyte involved in fluid balance in the brain. N-Acetyl-L-aspartic acid is also involved in energy production from glutamate in neuronal mitochondria. Further,