Relevant bibliographies by topics / Demyelinating diseases/Multiple sclerosis

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Demyelinating diseases/Multiple sclerosis'

Author: Grafiati
Published: 4 June 2021
Last updated: 15 February 2022

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Journal articles on the topic "Demyelinating diseases/Multiple sclerosis"

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Jellinger, K. A. "Multiple Sclerosis and Demyelinating Diseases." European Journal of Neurology 14, no. 4 (April 2007): e13-e13. http://dx.doi.org/10.1111/j.1468-1331.2007.01748.x.

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Vega-Riquer, Jose M., Gerardo Mendez-Victoriano, Raul A. Morales-Luckie, and Oscar Gonzalez-Perez. "Five Decades of Cuprizone, an Updated Model to Replicate Demyelinating Diseases." Current Neuropharmacology 17, no. 2 (January 7, 2019): 129–41. http://dx.doi.org/10.2174/1570159x15666170717120343.

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Introduction: Demyelinating diseases of the central nervous system (CNS) comprise a group of neurological disorders characterized by progressive (and eventually irreversible) loss of oligodendrocytes and myelin sheaths in the white matter tracts. Some of myelin disorders include: Multiple sclerosis, Guillain-Barré syndrome, peripheral nerve polyneuropathy and others. To date, the etiology of these disorders is not well known and no effective treatments are currently available against them. Therefore, further research is needed to gain a better understand and treat these patients. To accomplish this goal, it is necessary to have appropriate animal models that closely resemble the pathophysiology and clinical signs of these diseases. Herein, we describe the model of toxic demyelination induced by cuprizone (CPZ), a copper chelator that reduces the cytochrome and monoamine oxidase activity into the brain, produces mitochondrial stress and triggers the local immune response. These biochemical and cellular responses ultimately result in selective loss of oligodendrocytes and microglia accumulation, which conveys to extensive areas of demyelination and gliosis in corpus callosum, superior cerebellar peduncles and cerebral cortex. Remarkably, some aspects of the histological pattern induced by CPZ are similar to those found in multiple sclerosis. CPZ exposure provokes behavioral changes, impairs motor skills and affects mood as that observed in several demyelinating diseases. Upon CPZ removal, the pathological and histological changes gradually revert. Therefore, some authors have postulated that the CPZ model allows to partially mimic the disease relapses observed in some demyelinating diseases. Conclusion: for five decades, the model of CPZ-induced demyelination is a good experimental approach to study demyelinating diseases that has maintained its validity, and is a suitable pharmacological model for reproducing some key features of demyelinating diseases, including multiple sclerosis.
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Lan, Minghong, Xiaoyi Tang, Jie Zhang, and Zhongxiang Yao. "Insights in pathogenesis of multiple sclerosis: nitric oxide may induce mitochondrial dysfunction of oligodendrocytes." Reviews in the Neurosciences 29, no. 1 (December 20, 2017): 39–53. http://dx.doi.org/10.1515/revneuro-2017-0033.

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Abstract Demyelinating diseases, such as multiple sclerosis (MS), are kinds of common diseases in the central nervous system (CNS), and originated from myelin loss and axonal damage. Oligodendrocyte dysfunction is the direct reason of demyelinating lesions in the CNS. Nitric oxide (NO) plays an important role in the pathological process of demyelinating diseases. Although the neurotoxicity of NO is more likely mediated by peroxynitrite rather than NO itself, NO can impair oligodendrocyte energy metabolism through mediating the damaging of mitochondrial DNA, mitochondrial membrane and mitochondrial respiratory chain complexes. In the progression of MS, NO can mainly mediate demyelination, axonal degeneration and cell death. Hence, in this review, we extensively discuss endangerments of NO in oligodendrocytes (OLs), which is suggested to be the main mediator in demyelinating diseases, e.g. MS. We hypothesize that NO takes part in MS through impairing the function of monocarboxylate transporter 1, especially causing axonal degeneration. Then, it further provides a new insight that NO for OLs may be a reliable therapeutic target to ameliorate the course of demyelinating diseases.
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Lattanzi, Simona, Francesco Logullo, Paolo Di Bella, Mauro Silvestrini, and Leandro Provinciali. "Multiple sclerosis, solitary sclerosis or something else?" Multiple Sclerosis Journal 20, no. 14 (May 22, 2014): 1819–24. http://dx.doi.org/10.1177/1352458514535129.

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Background: Inflammatory demyelinating diseases of the central nervous system represent a wide spectrum of entities and their classification cannot currently be regarded complete. Objective: Our aim is to describe a series of patients presenting with progressive myelopathy associated to a single demyelinating lesion of the spinal cord. Methods: We identified the patients affected by chronic progressive spinal cord dysfunction related to a single spinal cord lesion not satisfying the diagnostic criteria for any of the currently defined diseases. Results: Seven females and one male were included. The median age at onset of symptoms was 53 years (range 42–68) and the median follow-up was 8 years (range 5–12). Brain and spinal magnetic resonance imaging (MRI) scans detected only one single, circumscribed, T2 hyperintense, non-longitudinally extensive lesion at level of cervico-medullary junction or cervical cord, in the absence of Gadolinium enhancement or swelling. Cerebrospinal fluid (CSF) examination displayed neither oligoclonal bands nor raised IgG index. A response to immunosuppressive agents was observed in some of the patients. Serial control brain and spinal MRI did not reveal accumulation of new lesions. Conclusion: New entities or variants should be included among the inflammatory demyelinating diseases of the central nervous system, and their characterization may have relevant prognostic and treatment implications.
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Goncharova, Z. A., and Y. Y. Pogrebnova. "Idiopathic inflammatory demyelining diseases: optimization of early diagnosis, predictors of the course." South Russian Journal of Therapeutic Practice 2, no. 2 (July 7, 2021): 80–87. http://dx.doi.org/10.21886/2712-8156-2021-2-2-80-87.

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Objective: to describe the clinical and epidemiological features of idiopathic inflammatory demyelinating diseases and to determine the factors influencing their course. Materials and methods: the study included 803 patients with idiopathic inflammatory demyelinating diseases using patient questionnaires and scales, laboratory and instrumental research methods. Statistical processing of the results was carried out using a point biserial coefficient and programs for analyzing large data arrays and machine learning. Results: a dynamic increase in the prevalence of some forms of idiopathic inflammatory demyelinating diseases was revealed, the difficulties of differential diagnosis of rare forms of demyelination and the need to create a unified version of their classification are reflected. In the studied population, the effectiveness of liquorological examination in the diagnosis of multiple sclerosis in the early stages of the disease was shown. It has been shown that the likelihood of developing highly active multiple sclerosis is influenced by both a genetic factor and concomitant inflammatory, allergic and autoimmune diseases, surgical interventions, dietary habits, childhood infections, and a history of pregnancy. Conclusions: given the complexity of the differential diagnosis of idiopathic inflammatory demyelinating diseases and the appointment of modifying therapy in multiple sclerosis in the early stages, it is necessary to create a combined classification and maintain a common register.
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Lewis, Steven L. "Multiple Approaches to Multiple Sclerosis (and Other Demyelinating Diseases)." CONTINUUM: Lifelong Learning in Neurology 22, no. 3 (June 2016): 721–22. http://dx.doi.org/10.1212/01.con.0000484469.69685.f2.

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Oleszak, Emilia L., J. Robert Chang, Herman Friedman, Christos D. Katsetos, and Chris D. Platsoucas. "Theiler's Virus Infection: a Model for Multiple Sclerosis." Clinical Microbiology Reviews 17, no. 1 (January 2004): 174–207. http://dx.doi.org/10.1128/cmr.17.1.174-207.2004.

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SUMMARY Both genetic background and environmental factors, very probably viruses, appear to play a role in the etiology of multiple sclerosis (MS). Lessons from viral experimental models suggest that many different viruses may trigger inflammatory demyelinating diseases resembling MS. Theiler's virus, a picornavirus, induces in susceptible strains of mice early acute disease resembling encephalomyelitis followed by late chronic demyelinating disease, which is one of the best, if not the best, animal model for MS. During early acute disease the virus replicates in gray matter of the central nervous system but is eliminated to very low titers 2 weeks postinfection. Late chronic demyelinating disease becomes clinically apparent approximately 2 weeks later and is characterized by extensive demyelinating lesions and mononuclear cell infiltrates, progressive spinal cord atrophy, and axonal loss. Myelin damage is immunologically mediated, but it is not clear whether it is due to molecular mimicry or epitope spreading. Cytokines, nitric oxide/reactive nitrogen species, and costimulatory molecules are involved in the pathogenesis of both diseases. Close similarities between Theiler's virus-induced demyelinating disease in mice and MS in humans, include the following: major histocompatibility complex-dependent susceptibility; substantial similarities in neuropathology, including axonal damage and remyelination; and paucity of T-cell apoptosis in demyelinating disease. Both diseases are immunologically mediated. These common features emphasize the close similarities of Theiler's virus-induced demyelinating disease in mice and MS in humans.
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Hardy, Todd A., W. Oliver Tobin, and Claudia F. Lucchinetti. "Exploring the overlap between multiple sclerosis, tumefactive demyelination and Baló’s concentric sclerosis." Multiple Sclerosis Journal 22, no. 8 (April 1, 2016): 986–92. http://dx.doi.org/10.1177/1352458516641776.

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The availability of magnetic resonance imaging (MRI) has led to increasing recognition that multiple sclerosis (MS), tumefactive demyelination (TD) and Baló’s concentric sclerosis (BCS) share many overlapping features. Baló-like lesions, which exhibit limited features of BCS, may represent an intermediate between BCS and typical MS demyelination. Lesions labeled as tumefactive are typically larger, but otherwise have much in common with conventional MS lesions, and TD and BCS lesions can also overlap. In this article, we explore the similarities between typical MS, TD and BCS cases, and reflect on the potential insights that intermediate or overlapping phenotypes may contribute towards an understanding of MS immunopathogenesis, and question whether these atypical forms of demyelination should be classified as separate demyelinating diseases, as different lesional manifestations of demyelination of any cause or as part of a spectrum with conventional MS.
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Yoon, Hye Hyun, Ji Young Park, Su Yeong Kim, Na Mi Lee, Dae Yong Yi, Sin Weon Yun, In Seok Lim, and Soo Ahn Chae. "Epidemiology of Demyelinating Diseases in Korean Pediatric Patients." Journal of Child Neurology 36, no. 2 (September 28, 2020): 141–47. http://dx.doi.org/10.1177/0883073820959543.

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The epidemiology of demyelinating diseases in the Korean pediatric population has not been reported to date. This study aimed to identify the epidemiology of demyelinating diseases in Korean children by using big data. The subjects were children (0-17 years old) diagnosed with acute-disseminated encephalomyelitis, multiple sclerosis, neuromyelitis optica, and Guillain-Barré syndrome enrolled in the Korean Health Insurance Review and Assessment Service (HIRA) from January 2010 to December 2017. Of 1722 enrolled children, 553 (32.1%) had acute-disseminated encephalomyelitis, 170 (9.9%) had multiple sclerosis, 68 (3.9%) had neuromyelitis optica, and 931 (54.1%) had Guillain-Barré syndrome. The male-female ratios were 1.47:1 in acute-disseminated encephalomyelitis, 1.43:1 in Guillain-Barré syndrome, 1:1.66 in multiple sclerosis, and 1:1.62 in neuromyelitis optica. Demyelinating diseases were most prevalent in summer. The prevalence differed by region, with 545 (31.6%) in Seoul and 298 (17.3%) in Gyeonggi. This study is the first to identify the incidence of demyelinating diseases in South Korea.
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Rostásy, Kevin, and Barbara Bajer-Kornek. "Paediatric multiple sclerosis and other acute demyelinating diseases." Current Opinion in Neurology 31, no. 3 (June 2018): 244–48. http://dx.doi.org/10.1097/wco.0000000000000562.

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Dissertations / Theses on the topic "Demyelinating diseases/Multiple sclerosis"

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Hogan, Vanessa E. "The role of mitochondira in demyelinating disease." Thesis, University of Newcastle Upon Tyne, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.493200.

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520 L $$aIn the CNS, myelination of axons is essential for the rapid conduction of impulses down the nerve. In demyelinated or failing axons however, conduction is less efficient and requires more energy. The principal function of mitochondria is to provide energy for the axon but in doing so they generate most of the intra-axonal reactive oxygen species (ROS). Therefore and increased energy requirement will promote an increased production of ROS which could lead to significant damage to essential DNA, proteins and lipids and could eventually damage the axon. This thesis investigates the mitochondrial involvement in axonal pathology in the CNS diseases, multiple sclerosis (MS), autosomal dominant optic atrophy (ADOA) and tosomal dominant optic atrophy with cataract (ADOAC).
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Matyszak, M. K. "Immune mediated inflammatory responses in the central nervous system." Thesis, University of Oxford, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.334846.

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Kerstetter, Fogle Amber E. "ROLE OF CHEMOKINES IN REGULATING OLIGODENDROCYTE DEVELOPMENT, ASTROGLIOSIS, AND DEMYELINATING DISEASES." Case Western Reserve University School of Graduate Studies / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=case1258139447.

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Teixeira, Carlos Augusto Ciarlini. "CaracterÃsticas clÃnicas e epidemiolÃgicas de 146 pacientes com esclerose mÃltipla acompanhados na cidade de Fortaleza, CE, Brasil, entre os anos 1979 e 2010." Universidade Federal do CearÃ, 2011. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=7515.

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nÃo hÃ
Para analisar a histÃria natural da Esclerose MÃltipla (EM) no estado do CearÃ, Brasil, o autor estuda retrospectivamente 146 pacientes diagnosticados por critÃrios de Poser e / ou McDonald-2010. CasuÃstica e mÃtodos: dados biogrÃficos, clÃnicos e para-clÃnicos obtidos em visitas ambulatoriais e nos surtos. Considera como desfechos de incapacidade os marcos EDSS 4, 6 e 7. Com software estatÃstico R ( RKWard 0.5.3 ) faz anÃlise descritiva, teste exato de Fisher (p < 0,05) e curvas de anÃlise de tempo atà o evento ( Kaplan-Meier). Mais de 75 % dos pacientes sÃo acompanhados durante atà 15 anos. Resultados: EM predomina no sexo feminino (80,82 %); tem inÃcio antes dos 30 anos de idade em 47,9 % dos casos. Pacientes com educaÃÃo de nÃvel superior (33,5 %) representam mais do dobro do esperado na populaÃÃo em geral. Nas avaliaÃÃes inicial e evolutiva predominam os sintomas sensitivos, motores e esfincterianos. Pacientes mais jovens e com evoluÃÃo recorrente â remitente atingem EDSS 4 apÃs maior intervalo de tempo. A proporÃÃo de casos de EM benigna à de 4,7 %. A taxa anualizada de surtos à 0,6. Os dois primeiros surtos da maioria dos pacientes ocorreram nos primeiros 3 anos. O tempo entre 1 e 2 surtos tem relaÃÃo positiva com o tempo para atingir EDSS 4, 6 e 7. A duraÃÃo da doenÃa atà o Ãbito (8 casos, 5,4 %) foi em mÃdia de 14,4 anos. PrevalÃncia de EM no estado do Cearà à estimada em 2,9 / 100.000 habitantes. ConclusÃo: As caracterÃsticas clÃnicas e evolutivas da EM, no estado do Cearà (latitude sul entre 2o 46â e 7o 52â), sÃo semelhantes Ãs observadas mundialmente.
In order to study the natural history of Multiple Sclerosis (MS) in the state of CearÃ, Brazil, the author retrospectively analyzes 146 patients diagnosed according to Poser and/or McDonald-2010 criteria. Cases and methods: biographical, clinical and para-clinical data collected on outpatient visits and at relapses. EDSS scores 4, 6 and 7 used as disability outcomes. Statistical software R (RKWard 0.5.3) used to perform descriptive analysis, Fisher exact test (p< 0,05) and time-to-the-event curves (Kaplan-Meier). Results: over 75 % of the patients followed for as long as 15 years; disease onset before 30 years of age in 47,9 %, with female sex preponderance (80.82 %). Patients with university education (33,5 %) are in high proportion when compared to the general population. Sensory, motor and sphincter complaints are the most common, in both initial and final examinations. Younger patients with relapsing-remitting MS took a longer time to reach EDSS 4. The proportion of benign MS cases was 4, 7 %. Annualized relapse rate was 0,6 . For most patients, the first two relapses took place in the initial three years of illness.Time between 1st. and 2nd relapses bears a positive relationship with time to reach EDSS 4, 6 and 7. Disease duration until death (8 cases , 5,4 %) was an average of 14,4 years. The prevalence of MS in the state of CearÃ, Brazil, is estimated as 2,9 / 100.000 inhabitants. Conclusion: Clinical course of MS in the state of CearÃ, Brazil (south latitudes between 2o 46â and 7o 52â ) is similar to that observed worldwide.
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Belzycki, Sari E. "Measurement of brain atrophy in pediatric patients with clinically isolated demyelinating syndromes and multiple sclerosis." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=112380.

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Brain atrophy has been used as a marker for disease progression in Multiple Sclerosis (MS). SIENA, an automated tool for measuring brain volume change, was tested to see whether MRI slice thickness and gap presence affect longitudinal atrophy measures. Isotropic global scan-rescan images were used to simulate 3 mm and 5 mm axial slice thicknesses with 1 and 2mm gaps, respectively. SIENA remained accurate and precise with increasing slice thickness and gap presence. Furthermore, symmetric pre-registration was crucial for scans with larger slice-thickness and gaps.
SIENA was used to observe atrophy in children who have experienced a Clinically Isolated Syndrome (CIS) of the type leading to MS (CIS-MS). Brain atrophy was present within the first three months after a CIS event, and then subsided over the rest of the year. If the first acute episode was excluded, there was no significant difference in atrophy rates between the CIS-MS group and the CIS group, and no significant difference between those with T2-weighted brain lesions versus those who had none.
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Caruana, P. "Visual psychophysics and magnetic resonance imaging in demyelinating disease of the visual system." Thesis, Keele University, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.245886.

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Riley, Victoria Jane. "The effect of cytokines on neurological exacerbations in multiple sclerosis and experimental demyelinating disease." Thesis, University of Cambridge, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.621588.

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Vana, Adam C. "The oligodendrocyte progenitor response to demyelination /." Download the dissertation in PDF, 2006. http://www.lrc.usuhs.mil/dissertations/pdf/vana2006.pdf.

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Kornfeld, Samantha F. "MiR-145-5p: Its Roles in Oligodendrocyte Differentiation and Its Contributions to the Pathophysiology of Demyelinating Disease." Thesis, Université d'Ottawa / University of Ottawa, 2020. http://hdl.handle.net/10393/40617.

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Multiple sclerosis (MS) is a debilitating disease in which demyelinated lesions form in the central nervous system (CNS). A specific microRNA, miR-145-5p, is dysregulated both in blood samples from RRMS patients and in chronic lesions from progressive MS patients. In the context of remyelination, miR-145-5p regulation may be important as it exhibits strong differential regulation in oligodendrocytes (OLs), the myelinating cells of the CNS, and is also expressed in other CNS glial cell types. Dysregulation of miR-145-5p may therefore play into pathologies observed in both relapsing-remitting (RRMS) and progressive MS. Using pre-clinical rodent models, we aimed to determine how altering normal expression of miR-145-5p specifically affects OL maturation, and how the dysregulation observed in MS may affect various aspects of disease. First using a miR-145 knockdown model in primary rat OLs, we found in vitro that miR-145-5p plays a role both in maintaining oligodendrocyte progenitor cells (OPCs) in their proliferative state and preventing premature differentiation to OLs and that knockdown of miR-145 in OLs enhanced their differentiation. These effects were due at least in part to miR-145-5p regulation of a critical myelin gene transcription factor. The effects of miR-145-5p were further assessed in a miR-145 knockout mouse model in vivo. Contrary to in vitro assays, enhanced myelination was not detectable during development in these animals, nor when remyelination was assessed using the cuprizone toxic model of acute demyelination. However, chronic cuprizone exposure resulted in striking remyelination and functional recovery in miR-145 deficient animals. Sparse remyelination in wild-type animals with chronic cuprizone exposure was concomitant with upregulation of miR-145-5p, which was not the case with acute exposure, identifying miR-145-5p dysregulation as a unique feature of chronic demyelination. Specific assessment of miR-145-5p overexpression in OLs in vitro resulted in severe differentiation deficits and eventual apoptosis, driven molecularly by altered expression of multiple pathways critical to successful OL differentiation and subsequent myelination. Finally, we induced an inflammatory model of demyelination, experimental autoimmune encephalomyelitis (EAE), in our miR-145 knockout mouse to assess the role of miR-145-5p in autoimmune-mediated myelin damage. The clinical severity of EAE in miR-145 deficient animals was reduced, and this was accompanied by reduced loss of myelin and lessened immune cell infiltration in miR-145 knockout spinal cords. Alterations in both astrocytic and microglial activation were detected with loss of miR-145, suggesting that improved clinical outcomes in this model may be underpinned by changes in EAE-mediated neuroinflammation. Collectively, these data suggest that miR-145-5p plays differing roles in both progressive and inflammatory MS, affecting multiple glial cell types in the CNS. Excitingly, loss of miR-145 expression in our mouse model of chronic demyelination allowed extensive remyelination and functional recovery following chronic demyelination, and in EAE improved clinical outcomes driven by underlying improvements in myelin retention and altered neuroinflammatory reactions. Thus, miR-145-5p merits further investigation as a potential therapeutic target to help overcome both remyelination failure in all forms of progressive MS and inflammation-driven demyelination in RRMS and early secondary progressive MS (SPMS).
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Kvarnström, Maria. "Mechanisms in inflammatory demyelinating diseases of the nervous system : immunological and methodological aspects /." Linköping : Linköpings universitet, 2005. http://www.bibl.liu.se/liupubl/disp/disp2005/med892s.pdf.

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Books on the topic "Demyelinating diseases/Multiple sclerosis"

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Rodriguez, Moses, ed. Advances in multiple Sclerosis and Experimental Demyelinating Diseases. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-73677-6.

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Satellite Symposium on Myelination and Demyelination: Implications for Multiple Sclerosis (1987 Vancouver, B.C.). Myelination and demyelination: Implications for multiple sclerosis. New York: Plenum Press, 1989.

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Demyelinating disorders of the central nervous system in childhood. Cambridge: Cambridge University Press, 2010.

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Rosner, Louis J. Multiple sclerosis. New York: Prentice Hall Press, 1987.

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Multiple sclerosis. London: Routledge, 1988.

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Gold, Susan Dudley. Multiple sclerosis. Parsippany, N.J: Crestwood House, 1997.

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Multiple sclerosis. Parsippany, N.J: Crestwood House, 1998.

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Understanding multiple sclerosis. Jackson: University Press of Mississippi, 2006.

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Rudick, Richard A., and Jeffrey A. Cohen. Multiple sclerosis therapeutics. 4th ed. Cambridge: Cambridge University Press, 2011.

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Multiple sclerosis therapeutics. 4th ed. Cambridge: Cambridge University Press, 2011.

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Book chapters on the topic "Demyelinating diseases/Multiple sclerosis"

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Weis, Serge, Michael Sonnberger, Andreas Dunzinger, Eva Voglmayr, Martin Aichholzer, Raimund Kleiser, and Peter Strasser. "Demyelinating Diseases: Multiple Sclerosis." In Imaging Brain Diseases, 1071–95. Vienna: Springer Vienna, 2019. http://dx.doi.org/10.1007/978-3-7091-1544-2_41.

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Leary, Siobhan, Gavin Giovannoni, Robin Howard, David Miller, and Alan Thompson. "Multiple Sclerosis and Demyelinating Diseases." In Neurology, 475–511. Chichester, UK: John Wiley & Sons, Ltd, 2016. http://dx.doi.org/10.1002/9781118486160.ch11.

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Bianchi, Valentina, and Carlo Pozzilli. "Coping and Multiple Sclerosis." In Neuropsychiatric Symptoms of Inflammatory Demyelinating Diseases, 121–37. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-18464-7_10.

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Defer, Gilles, and Pierre Branger. "Dementia in Multiple Sclerosis." In Neuropsychiatric Symptoms of Inflammatory Demyelinating Diseases, 257–69. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-18464-7_18.

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Magistrale, Giuseppe, and Ugo Nocentini. "Anxiety and Multiple Sclerosis." In Neuropsychiatric Symptoms of Inflammatory Demyelinating Diseases, 39–63. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-18464-7_4.

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Foley, Frederick W. "Psychology of Multiple Sclerosis." In Neuropsychiatric Symptoms of Inflammatory Demyelinating Diseases, 107–19. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-18464-7_9.

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Dulau, Cécile. "Social Cognition and Multiple Sclerosis." In Neuropsychiatric Symptoms of Inflammatory Demyelinating Diseases, 213–26. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-18464-7_15.

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Ruet, Aurélie. "Cognitive Impairment in Multiple Sclerosis." In Neuropsychiatric Symptoms of Inflammatory Demyelinating Diseases, 227–47. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-18464-7_16.

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Carta, Mauro Giovanni, Maria Francesca Moro, Giuseppina Trincas, Lorena Lorefice, Eleonora Cocco, and Maria Giovanna Marrosu. "Multiple Sclerosis and Bipolar Disorders." In Neuropsychiatric Symptoms of Inflammatory Demyelinating Diseases, 65–74. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-18464-7_5.

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Bendszus, Martin, and Brigitte Storch-Hagenlocher. "Multiple Sclerosis and Other Demyelinating Diseases." In Inflammatory Diseases of the Brain, 3–18. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/174_2012_787.

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Conference papers on the topic "Demyelinating diseases/Multiple sclerosis"

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Fanouriakis, A., K. Voumvourakis, M. Papathanasiou, T. Doskas, T. Karageorgas, D. Tseronis, D. Kassara, A. Erden, P. Katsimbri, and D. Boumpas. "FRI0269 “if it's not multiple sclerosis, look for a connective tissue disease”: atypical demyelinating disorders referred to a tertiary rheumatology centre." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.6438.

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Loizou, C. P., I. Seimenis, M. Pantziaris, T. Kasparis, E. C. Kyriacou, and C. S. Pattichis. "Texture image analysis of normal appearing white matter areas in Clinically Isolated Syndrome that evolved in demyelinating lesions in subsequent MRI scans: Multiple sclerosis disease evolution." In 2010 10th IEEE International Conference on Information Technology and Applications in Biomedicine (ITAB 2010). IEEE, 2010. http://dx.doi.org/10.1109/itab.2010.5687688.

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Bitoun, S., C. Verstuyft, C. Miceli-Richard, J.-M. Berthelot, C. Richez, C. Cauquil, C. Sordet, et al. "FRI0180 Multiple sclerosis risk-alleles study in patients with demyelinating side effects on anti tnf alpha therapy." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.4710.

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"Analyzing Chronic Diseases with Latent Growth Models: An Analysis of Multiple Sclerosis." In 2009 42nd Hawaii International Conference on System Sciences. IEEE, 2009. http://dx.doi.org/10.1109/hicss.2009.72.

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"HAPLOTYPE-BASED CLASSIFIERS TO PREDICT INDIVIDUAL SUSCEPTIBILITY TO COMPLEX DISEASES - An Example for Multiple Sclerosis." In International Conference on Bioinformatics Models, Methods and Algorithms. SciTePress - Science and and Technology Publications, 2012. http://dx.doi.org/10.5220/0003874003600366.

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Siegrist, Kyle W., James R. Chagdes, and Ryan M. Kramer. "Investigating the Nonlinear Dynamics of Human Balance Using Topological Data Analysis." In ASME 2019 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. American Society of Mechanical Engineers, 2019. http://dx.doi.org/10.1115/detc2019-98014.

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Abstract:
Abstract Understanding the mechanisms behind human balance has been a subject of interest as various postural instabilities have been linked to neuromuscular diseases (Parkinson’s, multiple sclerosis, and concussion). This paper presents a classification method for an individual’s postural stability and estimation of their neuromuscular feedback control parameters. The method uses a generated topological mapping between a subjects experimental data and a data set consisting of time series realizations generated using an inverted pendulum mathematical model of upright balance. The performance of the method is quantified using a time series realizations with known stability and neuromuscular control parameters. The method was found to have an overall sensitivity of 85.1% and a specificity of 91.9%. Furthermore, the method was most accurate when identifying limit cycle oscillations with a sensitivity of 91.1% and a specificity of 97.6%. Such a method has the capability of classifying an individual’s stability and revealing possible neuromuscular impairment related to balance control, ultimately providing useful information to clinicians for diagnostic and rehabilitation purposes.
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