scholarly journals Ozone therapy in ethidium bromide-induced demyelination in rats: possible protective effect [abstract]

2019 ◽  
Vol 3 (4) ◽  
Author(s):  
Mohga Samy
Keyword(s):  
Multiple Sclerosis ◽  
Protective Effect ◽  
Ethidium Bromide ◽  
Demyelinating Diseases ◽  
Immune Reactivity ◽  
Methyl Prednisolone ◽  
The Central Nervous System ◽  
Group 5 ◽  
Group 2 ◽  
Oxygen Groups

BACKGROUND: Multiple sclerosis is an autoimmune inflammatory disease of the central nervous system and it is characterized by excessive demyelination PURPOSE: The study aim to investigate the possible protective effect of ozone (O3) in ethidium bromide (EB) induced demyelination in rats either alone or in combination with corticosteroid in order to decreases the dose of steroid therapy. MATERIAL and METHODS: Rats were divided into 7 groups Group (1) normal control rats received saline. Group (2) sham-operated rats received saline. Group (3) sham operated rats received oxygen. Group (4) EB-treated rats received EB. Group (5) EB treated rats received oxygen. Group (6) EB treated rats received methyl prednisolone (MP) Group (7) EB treated rats received half the dose of MP concomitant with ozone. RESULTS: Significant improvement in the brain serotonin, dopamine, noradrenalin. A reduction of MDA,TNF-COX2 immune-reactivity was noticed in MP and oxygen groups . Furthermore, best amelioration was achieved by combining half the dose of methyl-prednisolone with ozone. CONCLUSION: We concluded that ozone has a protective effect on demyelination and can be used due to its protective effect in demyelinating diseases such as multiple sclerosis.

NMO-IgG and Devic's neuromyelitis optica: a French experience

2008 ◽  
Vol 14 (4) ◽  
pp. 440-445 ◽  
Author(s):  
Romain Marignier ◽  
Jérôme De Sèze ◽  
Sandra Vukusic ◽  
Françoise Durand-Dubief ◽  
Hélène Zéphir ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Staining Pattern ◽  
Transverse Myelitis ◽  
Group 4 ◽  
Acute Transverse Myelitis ◽  
Group 3 ◽  
Group 5 ◽  
Group 2 ◽  
Devic’S Neuromyelitis Optica ◽  
Group 1

Background A serum autoantibody biomarker, NMO-IgG has been recently described in patients with Devic's neuromyelitis optica (DNMO) and so called `high-risk' patients for this disease. Our objectives were to replicate the test and to assess its usefulness. Methods Indirect immunofluorescence with a substrate of adult rat cerebellum and midbrain was used to identify the distinctive NMO-IgG staining pattern. We tested masked sera from 26 patients with DNMO (group 1), 21 patients with idiopathic acute transverse myelitis (ATM) (group 2), 21 patients with bilateral and/or recurrent idiopathic optic neuritis (group 3), 52 patients with classical multiple sclerosis (MS) (group 4), 36 patients with HTLV-1 infection (group 5) and 7 patients with miscellaneous disorders (group 6). Results We identified a vascular staining pattern typical of NMO-IgG. This particular staining was observed in 14/26 samples in group 1, 7/21 in group 2 (positive only in longitudinally extensive acute transverse myelitis: 7/13), 4/21 in group 3 (with bilateral loss of vision in all seropositive cases), 5/52 in group 4 (none of them suggestive of DNMO), 0/36 in group 5 and 0/7 in group 6. Sensitivity of the test was 54% considering detection of DNMO (group 1), and specificity was respectively 94% and 90% when considering groups 4, 5 and 6 altogether or group 4 of MS patients only. Conclusion Detection of NMO-IgG is contributory to the distinction of DNMO and `DNMO high-risk' syndromes from MS. This test may allow earlier diagnosis and help therapeutic decisions. Multiple Sclerosis 2008; 14: 440—445. http://msj.sagepub.com

Demyelinating disorders of the central nervous system

2010 ◽  
pp. 4948-4963
Author(s):  
Siddharthan Chandran ◽  
Alastair Compston
Keyword(s):  
Multiple Sclerosis ◽  
Central Nervous System ◽  
Nervous System ◽  
Acute Disseminated Encephalomyelitis ◽  
Demyelinating Diseases ◽  
Demyelinating Disorder ◽  
System P ◽  
The Central Nervous System ◽  
Demyelinating Disorders ◽  
Brain And Spinal Cord

Clinicians suspect demyelination when episodes reflecting damage to white matter tracts within the central nervous system occur in young adults. The paucity of specific biological markers of discrete demyelinating syndromes places an emphasis on clinical phenotype—temporal and spatial patterns—when classifying demyelinating disorders. The diagnosis of multiple sclerosis, the most common demyelinating disorder, becomes probable when these symptoms and signs recur, involving different parts of the brain and spinal cord. Other important demyelinating diseases include post-infectious neurological disorders (acute disseminated encephalomyelitis), demyelination resulting from metabolic derangements (central pontine myelinosis), and inherited leucodystrophies that may present in children or in adults. Accepting differences in mechanism, presentation, and treatment, two observations can usefully be made when classifying demyelinating disorders. These are the presence or absence of inflammation, and the extent of focal vs. diffuse demyelination. Multiple sclerosis is prototypic for the former, whereas dysmyelinating disorders, such as leucodystrophies are representative of the latter....

scholarly journals Differential diagnosis of suspected multiple sclerosis: a consensus approach

2008 ◽  
Vol 14 (9) ◽  
pp. 1157-1174 ◽  
Author(s):  
DH Miller ◽  
BG Weinshenker ◽  
M Filippi ◽  
BL Banwell ◽  
JA Cohen ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Differential Diagnosis ◽  
Evidence Base ◽  
Demyelinating Diseases ◽  
Future Research ◽  
International Panel ◽  
The Central Nervous System ◽  
Definition Of ◽  
Demyelinating Disorders ◽  
Diagnosis Criteria

Background and objectives Diagnosis of multiple sclerosis (MS) requires exclusion of diseases that could better explain the clinical and paraclinical findings. A systematic process for exclusion of alternative diagnoses has not been defined. An International Panel of MS experts developed consensus perspectives on MS differential diagnosis. Methods Using available literature and consensus, we developed guidelines for MS differential diagnosis, focusing on exclusion of potential MS mimics, diagnosis of common initial isolated clinical syndromes, and differentiating between MS and non-MS idiopathic inflammatory demyelinating diseases. Results We present recommendations for 1) clinical and paraclinical red flags suggesting alternative diagnoses to MS; 2) more precise definition of “clinically isolated syndromes” (CIS), often the first presentations of MS or its alternatives; 3) algorithms for diagnosis of three common CISs related to MS in the optic nerves, brainstem, and spinal cord; and 4) a classification scheme and diagnosis criteria for idiopathic inflammatory demyelinating disorders of the central nervous system. Conclusions Differential diagnosis leading to MS or alternatives is complex and a strong evidence base is lacking. Consensus-determined guidelines provide a practical path for diagnosis and will be useful for the non-MS specialist neurologist. Recommendations are made for future research to validate and support these guidelines. Guidance on the differential diagnosis process when MS is under consideration will enhance diagnostic accuracy and precision.

scholarly journals Plasma complement biomarkers distinguish multiple sclerosis and neuromyelitis optica spectrum disorder

2016 ◽  
Vol 23 (7) ◽  
pp. 946-955 ◽  
Author(s):  
Svetlana Hakobyan ◽  
Sebastian Luppe ◽  
David RS Evans ◽  
Katharine Harding ◽  
Samantha Loveless ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Neuromyelitis Optica ◽  
Unmet Need ◽  
Area Under The Curve ◽  
Spectrum Disorder ◽  
Demyelinating Diseases ◽  
Neuromyelitis Optica Spectrum Disorder ◽  
Complement Proteins ◽  
Activation Products ◽  
The Central Nervous System

Background: Multiple sclerosis (MS) and neuromyelitis optica spectrum disorder (NMOSD) are autoimmune inflammatory demyelinating diseases of the central nervous system. Although distinguished by clinicoradiological and demographic features, early manifestations can be similar complicating management. Antibodies against aquaporin-4 support the diagnosis of NMOSD but are negative in some patients. Therefore, there is unmet need for biomarkers that enable early diagnosis and disease-specific intervention. Objective: We investigated whether plasma complement proteins are altered in MS and NMOSD and provide biomarkers that distinguish these diseases. Methods: Plasma from 54 NMOSD, 40 MS and 69 control donors was tested in multiplex assays measuring complement activation products and proteins. Using logistic regression, we tested whether combinations of complement analytes distinguished NMOSD from controls and MS. Results: All activation products were elevated in NMOSD compared to either control or MS. Four complement proteins (C1inh, C1s, C5 and FH) were higher in NMOSD compared to MS or controls. A model comprising C1inh and terminal complement complex (TCC) distinguished NMOSD from MS (area under the curve (AUC): 0.98), while C1inh and C5 distinguished NMOSD from controls (AUC: 0.94). Conclusion: NMOSD is distinguished from MS by plasma complement biomarkers. Selected complement analytes enable differential diagnosis. Findings support trials of anti-complement therapies in NMOSD.

scholarly journals Effects of multiple sclerosis in pregnant and post-birth: particularities of the disease activity

2021 ◽  
Author(s):  
Bianca Barbosa Araldi ◽  
Victor Hugo Gomes ◽  
Bruno Ludvig Vieira ◽  
Klesia Adayani Rodrigues ◽  
Andressa Gabrieli da Silva ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Disease Activity ◽  
Neurological Diseases ◽  
Neuroprotective Effect ◽  
Cumulative Effect ◽  
Demyelinating Diseases ◽  
Hormonal Changes ◽  
Neuroprotective Effects ◽  
Maternal Immune System ◽  
The Central Nervous System

Introduction: Demyelinating diseases are a heterogeneous group of neurological diseases related to autoimmunity whose representative is Multiple Sclerosis (MS). It is characterized by an immune-mediated demyelination of the central nervous system, with a typical outbreak and remission clinic. During pregnancy, a reduction in disease activity was noted due to immunomodulatory effects, and an increase in outbreaks in the puerperium. Thus, our goal is to demonstrate the relationship between pregnancy and MS. Methods: This is a systematic bibliographic review based on searching the SCIELO, PUBMED and UPTODATE databases using the words “Multiple Sclerosis”, “Pregnancy”, “Demyelinating diseases” and “Neurological Disorders”. Discussion: Pregnancy is responsible for numerous changes in the maternal body resulting from hormonal changes with an immunological and neuroprotective effect. Until the beginning of the 20th century, it was considered a risk factor or precipitator of outbreaks in these patients. In 1950, Tillmann et al. questioned him and concluded that pregnancy reduces the risk of outbreaks of the disease and that relapses were more associated with postpartum. The question is still raised by several authors, due to their interest in the search for intricate protective factors in the genesis and cure of the disease. It is believed that immunological changes in pregnancy tend to suppress the maternal immune system preventing fetal rejection, and together with gestational hormones, they are able to make neuronal tissue more resistant to inflammatory aggression and greater capacity for cell repair. In the puerperium, there was an increase in outbreaks of the disease, probably associated with a reduction in hormone levels, the effects of which are lost after the elimination of the fetus. Breastfeeding is not associated with the prevention or risk of new MS outbreaks. The frequency of outbreaks before conception is the only independent predictor of new post-term episodes. There is no consensus regarding the therapeutic approach in these pregnant women. Conclusion: Evidence supports the association between pregnancy, reduced activity of MS and increased activity in the 3 months postpartum, due to the probable loss of neuroprotective effects associated with hormones. Recommendations regarding the use of immunomodulator are suspended before conception (“washout”) until term. New evidence did not associate the use of interferon-β with abortion, cesarean section or low birth weight. There was a benefit of long-term parity with a cumulative effect on the patient’s immunohumor modulation.

Identification of a Val I 45 IIe substitution in the human myelin oligodendrocyte glycoprotein: lack of association with multiple sclerosis

1997 ◽  
Vol 3 (6) ◽  
pp. 377-381 ◽  
Author(s):  
D. Rodriguez ◽  
B. Della Gaspera ◽  
B. Zalc ◽  
J-J. Hauw ◽  
B. Fontaine ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Myelin Oligodendrocyte Glycoprotein ◽  
Demyelinating Diseases ◽  
Target Antigen ◽  
Restriction Enzyme Digestion ◽  
Autoimmune Encephalomyelitis ◽  
Potential Implication ◽  
The Central Nervous System ◽  
Major Target ◽  
Experimental Autoimmune

Myelin/oligodendrocyte glycoprotein (MOG) is a major target antigen in experimental autoimmune encephalomyelitis and it has been suggested that it may as well play a key role in the demyelination process in multiple sclerosis (MS). As MOG variants could be pathogenic in autoimmune demyelinating diseases of the central nervous system, we analysed the coding sequence of MOG in MS patients and described a G→A transition occurring in exon 3 of the human MOG gene. The mutation predicts that isoleucine substitutes for a valine at codon I 45 (Val 145 lle) in the transmembrane region of the protein. This is the first aminoacid substitution reported in human MOG. The polymorphism can be detected by restriction enzyme digestion of genomic DNA or reverse-transcribed PCR amplified products, making it a simple tool to detect a potential implication of MOG alleles in susceptibility to MS by association study. The analysis of 83 unrelated MS patients and 82 unrelated healthy controls showed that the polymorphism is found in similar proportions in MS patients (18%) and controls (14.6%). It is therefore unlikely that the MOG Val 145 lle variant is responsible for genetic susceptibility to MS.

Glial Precursor Cells in the Adult Human Brain

1998 ◽  
Vol 4 (4) ◽  
pp. 264-272 ◽  
Author(s):  
Neil Scolding
Keyword(s):  
Multiple Sclerosis ◽  
Experimental Data ◽  
Demyelinating Diseases ◽  
Culture Techniques ◽  
Myelin Sheaths ◽  
The Central Nervous System ◽  
Glial Precursor ◽  
Tissue Culture Techniques

Oligodendrocytes, the glial cells responsible for laying down and maintaining myelin sheaths in the central nervous system, were first described only 75 years ago. The lineage of these cells, and its relationship with that of the second type of macroglia, the astrocyte, was much studied in vivo and in situ in the rodent over the next 60 years. In the early 1980s, progress in oligodendrocyte biology was markedly amplified by the application of tissue culture techniques–-not without some element of controversy, although this is now largely resolved. Oligodendrocytes have always been given more attention than many other cells as a consequence of their role as a key target in human demyelinating diseases; in fact, few studies of rodent oligodendrocytes fail to draw conclusions regarding multiple sclerosis. Now, however, techniques for studying human glia and their lineage more directly have emerged, and differences in rodent and human oligodendrocyte biology are becoming apparent. It is increasingly clear that some caution must accompany the uncritical extrapolation of rodent experimental data to human oligodendrocyte biology and, indeed, to human disease.

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