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Background: Multiple Sclerosis is a myelin destroyer disease, which physical activity can be effective in improving it. Therefore, in the present study, the effect of swimming on oligodendrocytic cells and myelin tissue in rat brain of the Cuprizone model of MS disease is investigated. Methods: In this study, 21 male Wistar rats were randomly divided into Control groups, Cuprizone and Swim + Cuprizone. For the induction of MS, Cuprizone 0.6% were gavaged for one month. The group of Swim + Cuprizone swam at the same time with gavage. The training program included 4 weeks of swimming for 5 sessions per week and 30 minutes. Immunohistochemistry technique was used to determine the percentage of immature and mature oligodendrocytes and Luxol fast blue solution for evaluation of myelin density. Image j software and One-way ANOVA was used to analyze the findings. Results: The mean percentage of immature and mature oligodendrocytes and myelin density in the Swim+Cuprizone group was significantly higher than that of the Cuprizone group (p≤0.05). Conclusion: Swimming decreases destruction of the oligodendrocytes and myelin cells due to Cuprizone.

Multiple sclerosis is an autoimmune inflammatory disease that causes the destruction of myelin and axonal degeneration. Given that multiple sclerosis is one of the most common neurological diseases, especially in young people, this disease is one of the main public health concerns. Therefore, it is important to understand the molecular mechanisms involved in the development of MS. Many molecular mechanisms control the process of myelination in the nervous system, and any changes in these regulatory mechanisms lead to impaired myelination. Current therapies have focus on controling the immune mechanisms involved in the disease process and are therefore only effective in the early stages of the disease and have no effect on axonal remyelination. But, therapies that reinforce the remyelination process may delay or prevent disability. Some recent studies have investigated the role of key genes of the Hippo signaling pathway in the myelination process of myelinating glial cells. According to these studies, the activity of YAP1/TAZ and its negative regulation in the Hippo pathway via CRB3, a cellular polarization factor, regulates myelin sheath synthesis. Thus, dysregulation of these genes can play a major role in the pathogenesis of many diseases related to the nervous system. Because there is no comprehensive review of the relationship between the hippo signaling pathway and multiple sclerosis; in this study, in addition to a narrative review of MS and its predisposing factors, the Hippo pathway as a pathway implicated in the defect of the myelination process in MS was investigated. [ABSTRACT FROM AUTHOR]

Background: Multiple Sclerosis is a myelin destroyer disease, which physical activity can be effective in improving it. Therefore, in the present study, the effect of swimming on oligodendrocytic cells and myelin tissue in rat brain of the Cuprizone model of MS disease is investigated. Methods: In this study, 21 male Wistar rats were randomly divided into Control groups, Cuprizone and Swim + Cuprizone. For the induction of MS, Cuprizone 0.6% were gavaged for one month. The group of Swim + Cuprizone swam at the same time with gavage. The training program included 4 weeks of swimming for 5 sessions per week and 30 minutes. Immunohistochemistry technique was used to determine the percentage of immature and mature oligodendrocytes and Luxol fast blue solution for evaluation of myelin density. Image j software and One-way ANOVA was used to analyze the findings. Results: The mean percentage of immature and mature oligodendrocytes and myelin density in the Swim+Cuprizone group was significantly higher than that of the Cuprizone group (p≤0.05). Conclusion: Swimming decreases destruction of the oligodendrocytes and myelin cells due to Cuprizone. [ABSTRACT FROM AUTHOR]

Multiple sclerosis (MS) is a chronic inflammatory immune-mediated disease of the central nervous system. Despite extensive investigations, many aspects of etiology and pathophysiology remain unclear. In multiple sclerosis patients, immune system reacts against autologous proteins in the myelin membrane. Most evidences support the hypothesis that both genetic and environmental factors contribute to disease development. But after the failure of genetic findings to explain the reason for the unequal incidence of MS in identical twins, investigators focused further on environmental factors such as vitamin D deficiency, smoking, living in different latitudes and perhaps the most importantly the role of viruses in people whom are genetically susceptible to MS. There is increasing evidence that viruses may play important role in MS pathogenesis following environmental triggers. Recently, studies focused on the role of herpes virus family, especially Epstein-Barr virus, human herpes virus 6 (HHV-6) and Varicella Zoster virus, as the virus is prevalent in society. This review mainly focused on the identification of important viruses with key role in MS the mechanism behind pathogenesis and describes the animal models of MS. The results of researches are shown strong evidence of the virus or antibodies to viral components in active plaques in MS affected patients, but still cannot be stated with certainty that one or more specific viruses are simultaneously trigger the disease. Further studies are required to prove the pathogenesis of viruses in MS.

Background&Objective: Lead toxicity is a common popular problem. Many researches were performed about this toxicity both in-vivo and in-vitro since 100 years ago.Those studies showed that lead have toxic effects such as behavioral disorders, decrease of IQ and decrease of learning and memory. Also lead has neurotoxic effects such as decrease of neuronal density in visual cortex of monkey, cell death in hippocampus and decrease of acetylcolin in rat’s hippocampus. In this study we examin neurotoxic effects of lead on rat’s radial nerve because radial nerve is a mix nerve. Materials&Methods: 24 adult male rats were divided in six groups. Groups I and II received lead acetate 4% and 2%, groups III and IV received disttiled water and normal water for one month.After this time, we killed rats and exposed radial nerve from behind of arm.Then studied them with light and electron microscopy. Results: In experimental groups we saw decrease of myelin sheath diameter and decrease of nuclear density in schwann cell. Also we saw many granules in mitochondrial matrix, active macrophage, edema and disarrangement of myelin sheath layers. Conclusion: We suggest that lead neurophaty is due to schwann cell injury and this lesion lead to decrease of myelin sheath.

Background and purpose: Myelin-producing oligodendrocytes play a key role in supporting normal neuronal function of the mammalian central nervous system (CNS). Formation of myelinating oligodendrocytes from their precursors requires activation and coordination of a set of stage-specific transcriptional regulators that are important for the biosynthesis of myelin components. Olig2 plays an important role in oligodendrocyte differentiation, myelination and remyelination. Some studies indicated the importance of Vitamin B12 in the immunotherapies for MS patients. This study investigated the effects of Vitamin B12 on total protein concentration (TPC) and Olig2 expression in the cerebral cortex. Materials and methods: Thirty mice were divided into three groups (n=10 in each group). The first group received Vitamin B12 injections (50 μg dissolved in normal saline) once a week for three weeks. Normal saline injection was done for the second group and the third group was left without injection as the control group. In this study we investigated the role of vitamin B12 on TPC and Olig2 expression in the cerebral cortex using Bio-Rad protein assay based on the Bradford dye procedure and Western Blot, respectively. Results: The results showed that TPC and Olig2 expression in the cerebral cortex increased in the group injected with vitamin B12 compared with those of the control group. Conclusion: It is believed that vitamin B12 may play a key role in myelination in the CNS by increasing Olig2 expression and thus oligodendrocytes differentiation. [ABSTRACT FROM AUTHOR]

Background: Axon regeneration in adult CNS is limited by the presence of inhibitory proteins associated with myelin. Although blocking PKC activity attenuates the ability of CNS myelin to inhibit neurite outgrowth, the role as well as mechanisms underlying the remyelination inhibition in CNS are still largely unknown. Considering the role of PKC in axonal regeneration and the vulnerability of optic chiasm in multiple sclerosis (MS), we assessed the effect of PKC inhibition on remyelination of lysolecithin induced demyelinated optic chiasm. Materials and Methods: Demyelination was induced by stereotaxic intra-chiasmatic injection of 1μl lysolecithin (%1) in male mice. Intracerebroventricular daily injection of a PKC inhibitor (GO6976) was done for 14 days post-lesion. Demyelination and remyelination patterns in optic chiasm were confirmed through histological verification and electrophysiological study using Luxol fast blue staining and visual evoked potentials (VEP) recording, respectively. Results: In lysolecithin treated animals, demyelination was mostly marked at days 3 and 7 post-lesion and an incomplete remyelination occurred at day 14 post-lesion. VEP recording showed increased P-latency at the days 3 and 7 post-lesion while it partially decreased at day 14. Following the inhibition of PKC, while the extent of demyelination and P-latency slightly decreased at the days 3 and 7 post-lesion, it recovered at day 14. VEP recording data were confirmed by histological verification. Conclusion: Inhibition of PKC activity could represent a potential therapeutic approach for stimulating the remyelination process in the context of multiple sclerosis. [ABSTRACT FROM AUTHOR]

Multiple Sclerosis (MS) is a chronic, inflammatory demyelinating disorder of the central nervous system. In this disease, the immune system attacks myelin sheath in the areas of the brain and spinal cord known as the white matter. Despite extensive researches, the etiology of disease is still unknown. Epidemiological evidences and high levels of immunoglobulin G in the cerebrospinal fluid of patients suggest a role for infectious disease in the etiology of multiple sclerosis. In this paper, we review the recent findings regarding the most extensively studied bacteria and viruses in the etiology of multiple sclerosis. [ABSTRACT FROM AUTHOR]