Journal articles: '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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Korb, Pearce J., and Augusto Miravalle. "Coding in Multiple Sclerosis and Other Demyelinating Diseases." CONTINUUM: Lifelong Learning in Neurology 22, no. 3 (June 2016): 951–59. http://dx.doi.org/10.1212/con.0000000000000322.

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Iannetti, P., A. Spalice, U. Raucci, M. G. Marciani, F. Spanedda, G. Bernardi, G. Trasimeni, and G. F. Gualdi. "Primary CNS demyelinating diseases in childhood: multiple sclerosis." Child's Nervous System 12, no. 3 (March 1996): 149–54. http://dx.doi.org/10.1007/bf00266819.

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Iovino, Aniello, Francesco Aruta, Raffaele Dubbioso, Lucia Ruggiero, Stefano Tozza, Emanuele Spina, Fiore Manganelli, and Rosa Iodice. "Primary Progressive Multiple Sclerosis Under Anti-TNFα Treatment: A Case Report." Journal of Central Nervous System Disease 12 (January 2020): 117957352097382. http://dx.doi.org/10.1177/1179573520973820.

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Antagonists of tumour necrosis factor α (TNFα) are a common therapeutic choice for autoimmune diseases. Although they are effective and relatively safe, an increasing number of immune-mediated adverse events have been reported. Among these, neurological adverse effectsm such as consisting of demyelinating events in the central and peripheral nervous system were described. Demyelination of the central nervous system is a rare complication after treatment with TNFα antagonists. Here, we report a case of multiple sclerosis under treatment with TNFα antagonists and discuss its etiopathogenesis. This 45-year-old female patient developed signs and symptoms suggestive of primary progressive multiple sclerosis during treatment with adalinumab for nodular cystic acne, and magnetic resonance imaging of the patient showed typical lesions of demyelinating disease.

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Andreula, C. F. "The Main Neuroimmune Diseases in Childhood: Multiple Sclerosis and Acute Disseminated Encephalomyelitis." Rivista di Neuroradiologia 18, no. 3 (June 2005): 315–28. http://dx.doi.org/10.1177/197140090501800307.

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Demyelination is the hallmark of neuroimmune disease. It is caused by a breakdown of myelin already formed, relative sparing of myelin producing oligodendrocytes, neurons and astrocytes, and venous inflammation with perivenous infiltration. The neuroradiological investigation of choice in this setting is magnetic resonance (MR) due to its ability to monitor the neuropathological process. Acute disseminated encephalomyelitis (ADEM), also known as postinfectious or hyperergic encephalomyelitis, disseminated vasculoencephalomyelitis and perivenous encephalitis, is the commonest neuroimmune disorder of childhood. Neuroradiological investigation is highly sensitive for a diagnosis of demyelinating disease. MR is highly sensitive but not specific. Spectroscopy is useful for diagnosis: the reduction in axonal density leads to a decrease in N-acetylaspartate with a concomitant increase in choline and myoinositol due to glial proliferation. Spectroscopic findings positive for a decrease of NAA and an increase in choline during the first episode of demyelinating disease in adolescence are suggestive of an evolution to MS.

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Valero-Esquitino, Verónica, Kristin Lucht, Pawel Namsolleck, Florianne Monnet-Tschudi, Tobias Stubbe, Franziska Lucht, Meng Liu, et al. "Direct angiotensin type 2 receptor (AT2R) stimulation attenuates T-cell and microglia activation and prevents demyelination in experimental autoimmune encephalomyelitis in mice." Clinical Science 128, no. 2 (September 5, 2014): 95–109. http://dx.doi.org/10.1042/cs20130601.

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In experimental autoimmune encephalomyelitis in mice (a model for multiple sclerosis), direct angiotensin AT2R stimulation attenuated T-cell infiltration, microglia activation, spinal cord demyelination and neurological deficits suggesting the AT2R as potential drug target for treatment of demyelinating diseases.

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Koike, Haruki, and Masahisa Katsuno. "Macrophages and Autoantibodies in Demyelinating Diseases." Cells 10, no. 4 (April 8, 2021): 844. http://dx.doi.org/10.3390/cells10040844.

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Myelin phagocytosis by macrophages has been an essential feature of demyelinating diseases in the central and peripheral nervous systems, including Guillain–Barré syndrome (GBS), chronic inflammatory demyelinating polyneuropathy (CIDP), and multiple sclerosis (MS). The discovery of autoantibodies, including anti-ganglioside GM1 antibodies in the axonal form of GBS, anti-neurofascin 155 and anti-contactin 1 antibodies in typical and distal forms of CIDP, and anti-aquaporin 4 antibodies in neuromyelitis optica, contributed to the understanding of the disease process in a subpopulation of patients conventionally diagnosed with demyelinating diseases. However, patients with these antibodies are now considered to have independent disease entities, including acute motor axonal neuropathy, nodopathy or paranodopathy, and neuromyelitis optica spectrum disorder, because primary lesions in these diseases are distinct from those in conventional demyelinating diseases. Therefore, the mechanisms underlying demyelination caused by macrophages remain unclear. Electron microscopy studies revealed that macrophages destroy myelin as if they are the principal players in the demyelination process. Recent studies suggest that macrophages seem to select specific sites of myelinated fibers, including the nodes of Ranvier, paranodes, and internodes, for the initiation of demyelination in individual cases, indicating that specific components localized to these sites play an important role in the behavior of macrophages that initiate myelin phagocytosis. Along with the search for autoantibodies, the ultrastructural characterization of myelin phagocytosis by macrophages is a crucial step in understanding the pathophysiology of demyelinating diseases and for the future development of targeted therapies.

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Hofer, Livia S., Sara Mariotto, Sebastian Wurth, Sergio Ferrari, Chiara R. Mancinelli, Rachele Delogu, Salvatore Monaco, et al. "Distinct serum and cerebrospinal fluid cytokine and chemokine profiles in autoantibody-associated demyelinating diseases." Multiple Sclerosis Journal - Experimental, Translational and Clinical 5, no. 2 (April 2019): 205521731984846. http://dx.doi.org/10.1177/2055217319848463.

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Background Demyelinating diseases of the central nervous system associated with autoantibodies against aquaporin-4 and myelin-oligodendrocyte-glycoprotein are mediated by different immunopathological mechanisms compared to multiple sclerosis. Objective The purpose of this study was to evaluate serum and cerebrospinal fluid cytokine/chemokine profiles in patients with autoantibodies against aquaporin-4 or autoantibodies against myelin-oligodendrocyte-glycoprotein-associated demyelination compared to multiple sclerosis and autoimmune encephalitis. Methods Serum and cerebrospinal fluid cytokine/chemokine levels were analysed using Procartaplex Multiplex Immunoassays. First, we analysed a panel of 32 cytokines/chemokines in a discovery group (nine aquaporin-4-antibody seropositive, nine myelin oligodendrocyte glycoprotein-antibody seropositive, eight encephalitis, 10 multiple sclerosis). Significantly dysregulated cytokines/chemokines were validated in a second cohort (11 aquaporin-4-antibody seropositive, 18 myelin oligodendrocyte glycoprotein-antibody seropositive, 18 encephalitis, 33 multiple sclerosis). Results We found 11 significantly altered cytokines/chemokines in cerebrospinal fluid and serum samples in the discovery group (a proliferation-inducing ligand, fractalkine=CX3CL1, growth-regulated oncogene-α, interleukin-1 receptor antagonist, interleukin-6, interleukin-8=CXCL8, interleukin-10, interleukin-21, interferon-ɣ-induced protein-10=CXCL10, monokine induced by interferon-ɣ=CXCL9, macrophage inflammatory protein-1ß=CCL4). Most of these cytokines/chemokines were up-regulated in autoantibodies against aquaporin-4 or autoantibodies against myelin-oligodendrocyte-glycoprotein positive patients compared to multiple sclerosis. We confirmed these results for cerebrospinal fluid interleukin-6 and serum interleukin-8, growth-regulated oncogene-α, a proliferation-inducing ligand and macrophage inflammatory protein-1β in the validation set. Receiver-operating characteristic analysis revealed increased levels of cerebrospinal fluid interleukin-6, serum interleukin-8 and growth-regulated oncogene-α in most patients with autoantibody-associated neurological diseases. Conclusion This study suggests that distinctive cerebrospinal fluid and serum cytokine/chemokine profiles are associated with autoantibody-mediated demyelination, but not with multiple sclerosis.

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Rodney, Cady, Sherriann Rodney, and Richard M. Millis. "Vitamin D and Demyelinating Diseases: Neuromyelitis Optica (NMO) and Multiple Sclerosis (MS)." Autoimmune Diseases 2020 (January 19, 2020): 1–9. http://dx.doi.org/10.1155/2020/8718736.

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Vitamin D deficiency is prevalent in all ages regardless of climate or geographical location and evidence is emerging that the incidence of autoimmune diseases is increasing worldwide. Women make up a large proportion of autoimmune disease diagnoses, underscoring the importance of fully elucidating the complex synergistic relationships between estrogens and vitamin D. Vitamin D receptor-activating drugs appear to enhance remyelination in patients diagnosed with multiple sclerosis (MS) and other demyelinating diseases such as neuromyelitis optica (NMO). This review is intended to update health practitioners about the potential role of vitamin D deficiency demyelination and to motivate future research on dietary recommendations for vitamin D in preventing and treating demyel1nating diseases.

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Lopes Silva, Rita. "Desafios no Diagnóstico e Tratamento da Esclerose Múltipla Pediátrica." Acta Médica Portuguesa 29, no. 7-8 (August 31, 2016): 419. http://dx.doi.org/10.20344/amp.8054.

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Tanaka, Tatsuhide, and Shigetaka Yoshida. "Mechanisms of remyelination: recent insight from experimental models." Biomolecular Concepts 5, no. 4 (August 1, 2014): 289–98. http://dx.doi.org/10.1515/bmc-2014-0015.

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AbstractOligodendrocytes and myelin play essential roles in the vertebrate central nervous system. Demyelination disrupts saltatory nerve conduction, leading to axonal degeneration and neurological disabilities. Remyelination is a regenerative process that replaces lost myelin. However, remyelination is disrupted in demyelinating diseases such as multiple sclerosis, at least partially, due to the failure of oligodendrocyte precursor cells to differentiate into myelinating oligodendrocytes. Understanding the molecular and cellular mechanisms that impact the differentiation of oligodendrocytes and myelination may help in the development of novel therapeutic strategies for demyelinating diseases. In this review, we focus on the molecular mechanisms controlling the differentiation of oligodendrocytes during remyelination, and we discuss the function of astrocytes and microglia in animal models of demyelinating diseases.

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Mehanna, Raja, and Joseph Jankovic. "Movement disorders in multiple sclerosis and other demyelinating diseases." Journal of the Neurological Sciences 328, no. 1-2 (May 2013): 1–8. http://dx.doi.org/10.1016/j.jns.2013.02.007.

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Suarez-Cedeno, Gerson, and Raja Mehanna. "Movement Disorders in Multiple Sclerosis and Other Demyelinating Diseases." Neurologist 26, no. 5 (September 2021): 161–66. http://dx.doi.org/10.1097/nrl.0000000000000333.

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Matas, Sandro Luiz de Andrade, Felipe von Glehn, Gustavo Bruniera Peres Fernandes, and Carlos Augusto Senne Soares. "Cerebrospinal fluid analysis in the context of CNS demyelinating diseases." Arquivos de Neuro-Psiquiatria 71, no. 9B (September 2013): 685–88. http://dx.doi.org/10.1590/0004-282x20130151.

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The central nervous system demyelinating diseases are a group of disorders with different etiologies, characterized by inflammatory lesions that are associated with loss of myelin and eventually axonal damage. In this group the most studied ones are multiple sclerosis (MS), neuromyelitis optic (NMO) and acute disseminated encephalomyelitis (ADEM). The cerebrospinal fluid is essential to differentiate between these different syndromes and to define multiple sclerosis, helping to assess the probability of Clinical Isolated Syndrome turn into multiple sclerosis.

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Takai, Yoshiki, Tatsuro Misu, Kimihiko Kaneko, Norio Chihara, Koichi Narikawa, Satoko Tsuchida, Hiroya Nishida, et al. "Myelin oligodendrocyte glycoprotein antibody-associated disease: an immunopathological study." Brain 143, no. 5 (May 1, 2020): 1431–46. http://dx.doi.org/10.1093/brain/awaa102.

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Abstract Conformation-sensitive antibodies against myelin oligodendrocyte glycoprotein (MOG) are detectable in patients with optic neuritis, myelitis, opticomyelitis, acute or multiphasic disseminated encephalomyelitis (ADEM/MDEM) and brainstem/cerebral cortical encephalitis, but are rarely detected in patients with prototypic multiple sclerosis. So far, there has been no systematic study on the pathological relationship between demyelinating lesions and cellular/humoral immunity in MOG antibody-associated disease. Furthermore, it is unclear whether the pathomechanisms of MOG antibody-mediated demyelination are similar to the demyelination patterns of multiple sclerosis, neuromyelitis optica spectrum disorders (NMOSD) with AQP4 antibody, or ADEM. In this study, we immunohistochemically analysed biopsied brain tissues from 11 patients with MOG antibody-associated disease and other inflammatory demyelinating diseases. Patient median onset age was 29 years (range 9–64), and the median interval from attack to biopsy was 1 month (range 0.5–96). The clinical diagnoses were ADEM (n = 2), MDEM (n = 1), multiple brain lesions without encephalopathy (n = 3), leukoencephalopathy (n = 3) and cortical encephalitis (n = 2). All these cases had multiple/extensive lesions on MRI and were oligoclonal IgG band-negative. Most demyelinating lesions in 10 of 11 cases showed a perivenous demyelinating pattern previously reported in ADEM (153/167 lesions) and a fusion pattern (11/167 lesions) mainly in the cortico-medullary junctions and white matter, and only three lesions in two cases showed confluent demyelinated plaques. In addition, 60 of 167 demyelinating lesions (mainly in the early phase) showed MOG-dominant myelin loss, but relatively preserved oligodendrocytes, which were distinct from those of AQP4 antibody-positive NMOSD exhibiting myelin-associated glycoprotein-dominant oligodendrogliopathy. In MOG antibody-associated diseases, MOG-laden macrophages were found in the perivascular spaces and demyelinating lesions, and infiltrated cells were abundant surrounding multiple blood vessels in and around the demyelinating lesions, mainly consisting of macrophages (CD68; 1814 ± 1188 cells/mm2), B cells (CD20; 468 ± 817 cells/mm2), and T cells (CD3; 2286 ± 1951 cells/mm2), with CD4-dominance (CD4+ versus CD8+; 1281 ± 1196 cells/mm2 versus 851 ± 762 cells/mm2, P < 0.01). Humoral immunity, evidenced by perivascular deposits of activated complements and immunoglobulins, was occasionally observed in some MOG antibody-associated demyelinating lesions, and the frequency was much lower than that in AQP4 antibody-positive NMOSD. Subpial lesions with perivenous demyelination were observed in both ADEM and cortical encephalitis. Our study suggests that ADEM-like perivenous inflammatory demyelination with MOG-dominant myelin loss is a characteristic finding of MOG antibody-associated disease regardless of whether the diagnostic criteria of ADEM are met. These pathological features are clearly different from those of multiple sclerosis and AQP4 antibody-positive NMOSD, suggesting an independent autoimmune demyelinating disease entity.

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Imitola, Jaime, Evan Y. Snyder, and Samia J. Khoury. "Genetic programs and responses of neural stem/progenitor cells during demyelination: potential insights into repair mechanisms in multiple sclerosis." Physiological Genomics 14, no. 3 (August 15, 2003): 171–97. http://dx.doi.org/10.1152/physiolgenomics.00021.2002.

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In recent years, it has become evident that the adult mammalian CNS contains a population of neural stem cells (NSCs) described as immature, undifferentiated, multipotent cells, that may be called upon for repair in neurodegenerative and demyelinating diseases. NSCs may give rise to oligodendrocyte progenitor cells (OPCs) and other myelinating cells. This article reviews recent progress in elucidating the genetic programs and dynamics of NSC and OPC proliferation, differentiation, and apoptosis, including the response to demyelination. Emerging knowledge of the molecules that may be involved in such responses may help in the design of future stem cell-based treatment of demyelinating diseases such as multiple sclerosis.

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Lampron, Antoine, Antoine Larochelle, Nathalie Laflamme, Paul Préfontaine, Marie-Michèle Plante, Maria Gabriela Sánchez, V. Wee Yong, Peter K. Stys, Marie-Ève Tremblay, and Serge Rivest. "Inefficient clearance of myelin debris by microglia impairs remyelinating processes." Journal of Experimental Medicine 212, no. 4 (March 16, 2015): 481–95. http://dx.doi.org/10.1084/jem.20141656.

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An imbalance between remyelinating and demyelinating rates underlies degenerative processes in demyelinating diseases such as multiple sclerosis. An optimal therapeutic strategy would be to stimulate remyelination while limiting demyelination. Although accumulation of myelin debris impairs remyelination, the mechanisms regulating the clearance of such debris by mononuclear phagocytic cells are poorly understood. We demonstrate that after cuprizone intoxication, CCR2-dependent infiltration of mouse bone marrow–derived cells is abundant in demyelinating areas, but that these cells do not impact demyelination. However, in CX3CR1-deficient mice, the clearance of myelin debris by microglia was blocked greatly, affecting the integrity of the axon and myelin sheaths and thus preventing proper remyelination. These results highlight the crucial role played by CX3CR1 in myelin removal and show that there can be no efficient remyelination after a primary demyelinating insult if myelin clearance by microglia is impaired.

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Bright, John J., Moses Rodriguez, and Subramaniam Sriram. "Differential Influence of Interleukin-12 in the Pathogenesis of Autoimmune and Virus-Induced Central Nervous System Demyelination." Journal of Virology 73, no. 2 (February 1, 1999): 1637–39. http://dx.doi.org/10.1128/jvi.73.2.1637-1639.1999.

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ABSTRACT Experimental allergic encephalomyelitis (EAE) and Theiler’s murine encephalomyelitis virus (TMEV) disease are two demyelinating diseases of the central nervous system (CNS) that serve as animal models for multiple sclerosis. Th1 cells are thought to play a role in the pathogenesis of CNS demyelination in both these diseases. We show here the differential influence of interleukin 12, a critical cytokine for the development of Th1 cells in EAE and TMEV disease.

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Brugarolas, Pedro, Daniel S. Reich, and Brian Popko. "Detecting Demyelination by PET: The Lesion as Imaging Target." Molecular Imaging 17 (January 1, 2018): 153601211878547. http://dx.doi.org/10.1177/1536012118785471.

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Noninvasive imaging of demyelination and remyelination is critical for diagnosis and clinical management of demyelinating diseases. Positron emission tomography (PET) has the potential to complement magnetic resonance imaging (MRI) by providing a quantitative measure specific to demyelination. In Brugarolas et al’s study 1 , we describe the development of the first PET tracer for voltage-gated K+ channels based on a clinically approved drug for multiple sclerosis that can be used for imaging demyelination in animal models.

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Kira, Jun-ichi. "Recent progress in multiple sclerosis research: astrocytopathy in demyelinating diseases." Rinsho Shinkeigaku 50, no. 11 (2010): 788–93. http://dx.doi.org/10.5692/clinicalneurol.50.788.

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Lucchinetti, Claudia. "Multiple Sclerosis and the Spectrum of CNS Inflammatory Demyelinating Diseases." Seminars in Neurology 28, no. 1 (February 2008): 003–6. http://dx.doi.org/10.1055/s-2007-1019123.

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Kishore, Abhinoy, Anurag Kanaujia, Soma Nag, A. M. Rostami, Lawrence C. Kenyon, Kenneth S. Shindler, and Jayasri Das Sarma. "Different Mechanisms of Inflammation Induced in Virus and Autoimmune-Mediated Models of Multiple Sclerosis in C57BL6 Mice." BioMed Research International 2013 (2013): 1–9. http://dx.doi.org/10.1155/2013/589048.

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Multiple sclerosis (MS) is an inflammatory demyelinating disease of the human central nervous system (CNS). Neurotropic demyelinating strain of MHV (MHV-A59 or its isogenic recombinant strain RSA59) induces MS-like disease in mice mediated by microglia, along with a small population of T cells. The mechanism of demyelination is at least in part due to microglia-mediated myelin stripping, with some direct axonal injury. Immunization with myelin oligodendrocyte glycoprotein (MOG) induces experimental autoimmune encephalomyelitis (EAE), a mainly CD4+T-cell-mediated disease, although CD8+T cells may play a significant role in demyelination. It is possible that both autoimmune and nonimmune mechanisms such as direct viral toxicity may induce MS. Our study directly compares CNS pathology in autoimmune and viral-induced MS models. Mice with viral-induced and EAE demyelinating diseases demonstrated similar patterns and distributions of demyelination that accumulated over the course of the disease. However, significant differences in acute inflammation were noted. Inflammation was restricted mainly to white matter at all times in EAE, whereas inflammation initially largely involved gray matter in acute MHV-induced disease and then is subsequently localized only in white matter in the chronic disease phase. The presence of dual mechanisms of demyelination may be responsible for the failure of immunosuppression to promote long-term remission in many MS patients.

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López-Guerrero, José Antonio, Inés Ripa, Sabina Andreu, and Raquel Bello-Morales. "The Role of Extracellular Vesicles in Demyelination of the Central Nervous System." International Journal of Molecular Sciences 21, no. 23 (November 30, 2020): 9111. http://dx.doi.org/10.3390/ijms21239111.

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It is being increasingly demonstrated that extracellular vesicles (EVs) are deeply involved in the physiology of the central nervous system (CNS). Processes such as synaptic activity, neuron-glia communication, myelination and immune response are modulated by EVs. Likewise, these vesicles may participate in many pathological processes, both as triggers of disease or, on the contrary, as mechanisms of repair. EVs play relevant roles in neurodegenerative disorders such as Alzheimer’s or Parkinson’s diseases, in viral infections of the CNS and in demyelinating pathologies such as multiple sclerosis (MS). This review describes the involvement of these membrane vesicles in major demyelinating diseases, including MS, neuromyelitis optica, progressive multifocal leukoencephalopathy and demyelination associated to herpesviruses.

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Das Sarma, Jayasri. "A Mechanism of Virus-Induced Demyelination." Interdisciplinary Perspectives on Infectious Diseases 2010 (2010): 1–28. http://dx.doi.org/10.1155/2010/109239.

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Myelin forms an insulating sheath surrounding axons in the central and peripheral nervous systems and is essential for rapid propagation of neuronal action potentials. Demyelination is an acquired disorder in which normally formed myelin degenerates, exposing axons to the extracellular environment. The result is dysfunction of normal neuron-to-neuron communication and in many cases, varying degrees of axonal degeneration. Numerous central nervous system demyelinating disorders exist, including multiple sclerosis. Although demyelination is the major manifestation of most of the demyelinating diseases, recent studies have clearly documented concomitant axonal loss to varying degrees resulting in long-term disability. Axonal injury may occur secondary to myelin damage (outside-in model) or myelin damage may occur secondary to axonal injury (inside-out model). Viral induced demyelination models, has provided unique imminent into the cellular mechanisms of myelin destruction. They illustrate mechanisms of viral persistence, including latent infections, virus reactivation and viral-induced tissue damage. These studies have also provided excellent paradigms to study the interactions between the immune system and the central nervous system (CNS). In this review we will discuss potential cellular and molecular mechanism of central nervous system axonal loss and demyelination in a viral induced mouse model of multiple sclerosis.

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Belfkih, Rachid, Omar Ghomari Khayat, Hind H’daidane, and Fatima Zahra El Amrani. "Pseudotumoral Demyelinating Lesions: A Presentation of Acute Disseminated Encephalomyelitis." Case Reports in Neurology 13, no. 2 (May 27, 2021): 289–96. http://dx.doi.org/10.1159/000515174.

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Pseudotumoral forms of demyelination are related to central nervous system demyelinating disorders, usually considered to be an atypical presentation of multiple sclerosis including its different varieties such as Balo’s, Schilder’s, and Marburg diseases. These lesions could also be seen in myelin oligodendrocyte glycoprotein antibody-associated demyelination, acute disseminated encephalomyelitis (ADEM), and neuromyelitis optica spectrum disorder. The pseudotumoral aspect may be mistakenly considered as an abscess or a cancerous tumor, in which case, patients could endure unnecessary possibly harmful brain biopsy and have a delay in their disease diagnostics and management. Once latter differential diagnosis is discarded, pseudotumoral demyelination prompts uncertainties concerning the nature of the underlying demyelinating condition as prognosis and management differ from multiple sclerosis to other syndromes, especially whether a chronic treatment is needed or not. In this case report, we present a 35-year-old male patient hospitalized in the department of neurology for a rapidly progressive onset of encephalopathy and polyfocal neurological deficits, with pseudotumoral lesions shown on brain MRI. On further investigations, ADEM was the more likely diagnosis that could fit the patient’s clinical and radiological presentation. Thence, he was put on high dose of intravenous corticosteroids, with a followed good recovery within the first week of the treatment.

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Sun, Lei, Elphine Telles, Molly Karl, Fengdong Cheng, Noreen Luetteke, Eduardo M. Sotomayor, Robert H. Miller, and Edward Seto. "Loss of HDAC11 ameliorates clinical symptoms in a multiple sclerosis mouse model." Life Science Alliance 1, no. 5 (September 24, 2018): e201800039. http://dx.doi.org/10.26508/lsa.201800039.

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Multiple sclerosis (MS) is a chronic, immune-mediated, demyelinating disease of the central nervous system (CNS). There is no known cure for MS, and currently available drugs for managing this disease are only effective early on and have many adverse side effects. Results from recent studies suggest that histone deacetylase (HDAC) inhibitors may be useful for the treatment of autoimmune and inflammatory diseases such as MS. However, the underlying mechanisms by which HDACs influence immune-mediated diseases such as MS are unclear. More importantly, the question of which specific HDAC(s) are suitable drug targets for the potential treatment of MS remains unanswered. Here, we investigate the functional role of HDAC11 in experimental autoimmune encephalomyelitis, a mouse model for MS. Our results indicate that the loss of HDAC11 in KO mice significantly reduces clinical severity and demyelination of the spinal cord in the post-acute phase of experimental autoimmune encephalomyelitis. The absence of HDAC11 leads to reduced immune cell infiltration into the CNS and decreased monocytes and myeloid DCs in the chronic progressive phase of the disease. Mechanistically, HDAC11 controls the expression of the pro-inflammatory chemokine C–C motif ligand 2 (CCL2) gene by enabling the binding of PU.1 transcription factor to the CCL2 promoter. Our results reveal a novel pathophysiological function for HDAC11 in CNS demyelinating diseases, and warrant further investigations into the potential use of HDAC11-specific inhibitors for the treatment of chronic progressive MS.

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Vargas-Lowy, David, and Tanuja Chitnis. "Pathogenesis of Pediatric Multiple Sclerosis." Journal of Child Neurology 27, no. 11 (September 5, 2012): 1394–407. http://dx.doi.org/10.1177/0883073812456084.

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Onset of multiple sclerosis in childhood occurs in 3-5% of patients. There is limited, but growing knowledge about the underlying pathobiology of pediatric MS. It is crucial to better understand this area in order to address central questions in the field: 1) Can pediatric multiple sclerosis inform us about factors related to disease initiation and propagation? 2) What are the biomarkers of disease course in pediatric multiple sclerosis; 3) Does pediatric multiple sclerosis pathogenesis differ from adult-onset multiple sclerosis; 4) How can we optimize treatment in pediatric demyelinating diseases? 5) Can pediatric multiple sclerosis provide insights into the environmental risk factors for multiple sclerosis in general? Here we review the current knowledge of the pathogenesis of multiple sclerosis in children, and address the five questions raised above.

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Mazhar, Faizan, and Nafis Haider. "Some Unique Considerations in Treatment of Multiple Sclerosis." Asian Journal of Pharmaceutical Research and Health Care 8, no. 3 (June 23, 2016): 72. http://dx.doi.org/10.18311/ajprhc/2016/3909.

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Multiple sclerosis is one of several diseases described as demyelinating because it causes damage to the myelin sheath. The presence of additional medical condition like pregnancy, osteoporosis and infections is common with multiple sclerosis that adversely affects the health outcomes. The treatment of MS becomes more complex when compounded by these existing additional medical condition. This review highlight important pharmacotherapeutic considerations in treatment of MS in these special patient population.

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Gacem, Nadjet, and Brahim Nait-Oumesmar. "Oligodendrocyte Development and Regenerative Therapeutics in Multiple Sclerosis." Life 11, no. 4 (April 9, 2021): 327. http://dx.doi.org/10.3390/life11040327.

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Myelination by oligodendrocytes (OLs) is an important biological process essential for central nervous system (CNS) development and functions. Oligodendroglial lineage cells undergo several morphological and molecular changes at different stages of their lineage progression into myelinating OLs. The transition steps of the oligodendrocyte progenitor cells (OPCs) to myelinating oligodendrocytes are defined by a specific pattern of regulated gene expression, which is under the control of coordinated signaling pathways. Any abnormal development, loss or failure of oligodendrocytes to myelinate axons can lead to several neurodegenerative diseases like multiple sclerosis (MS). MS is characterized by inflammation and demyelination, and current treatments target only the immune component of the disease, but have little impact on remyelination. Recently, several pharmacological compounds enhancing remyelination have been identified and some of them are in clinical trials. Here, we will review the current knowledge on oligodendrocyte differentiation, myelination and remyelination. We will focus on MS as a pathological condition, the most common chronic inflammatory demyelinating disease of the CNS in young adults.

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McQualter, Jonathan L., Rima Darwiche, Christine Ewing, Manabu Onuki, Thomas W. Kay, John A. Hamilton, Hugh H. Reid, and Claude C. A. Bernard. "Granulocyte Macrophage Colony-Stimulating Factor." Journal of Experimental Medicine 194, no. 7 (September 24, 2001): 873–82. http://dx.doi.org/10.1084/jem.194.7.873.

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Experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis, can be induced by immunization with a number of myelin antigens. In particular, myelin oligodendrocyte glycoprotein, a central nervous system (CNS)-specific antigen expressed on the myelin surface, is able to induce a paralytic MS-like disease with extensive CNS inflammation and demyelination in several strains of animals. Although not well understood, the egress of immune cells into the CNS in EAE is governed by a complex interplay between pro and antiinflammatory cytokines and chemokines. The hematopoietic growth factor, granulocyte macrophage colony-stimulating factor (GM-CSF), is considered to play a central role in maintaining chronic inflammation. The present study was designed to investigate the previously unexplored role of GM-CSF in autoimmune-mediated demyelination. GM-CSF−/− mice are resistant to EAE, display decreased antigen-specific proliferation of splenocytes, and fail to sustain immune cell infiltrates in the CNS, thus revealing key activities for GM-CSF in the development of inflammatory demyelinating lesions and control of migration and/or proliferation of leukocytes within the CNS. These results hold implications for the pathogenesis of inflammatory and demyelinating diseases and may provide the basis for more effective therapies for inflammatory diseases, and more specifically for multiple sclerosis.

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Kaufman, Michael. "Juvenile Metachromatic Leukodystrophy Mimicking Relapsing-Remitting Multiple Sclerosis." International Journal of MS Care 8, no. 4 (January 1, 2006): 141–43. http://dx.doi.org/10.7224/1537-2073-8.4.141.

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Some cases of late-onset metachromatic leukodystrophy (MLD), which typically presents as a peripheral neuropathy, may present as a rapidly progressive central nervous system demyelinating disorder. This case report describes an important diagnostic and treatment dilemma: Are multiple sclerosis and MLD really two diseases, and should MLD be considered and treated as an autoimmune disorder?

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Kirk, J., and A.-L. Zhou. "Viral Infection at the Blood-Brain Barrier in Multiple Sclerosis: – An Ultrastructural Study of Tissues from a Uk Regional Brain Bank." Multiple Sclerosis Journal 1, no. 4 (February 1996): 242–52. http://dx.doi.org/10.1177/135245859600100410.

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Although viral infections are often invoked as environmental factors in the aetiology and pathogenesis of multiple sclerosis (MS) it is only recently that a specific, indirect, cytokine-mediated mechanism for triggering of relapses during viral infections has been demonstrated. It is not yet clear however whether this indirect mechanism can account for all reported viral associations with the aetiopathogenesis of MS. A direct causal role of central nervous system (CNS) viral infection in MS has largely been discounted following repeated failures to demonstrate virus within the oligodendrocyte-myelin unit In the light of increasing evidence of blood-brain barrier (BBB) dysfunction in MS and to further explore the issue of possible viral involvement in MS, an ultrastructural search for viruses was undertaken in the CNS microvasculature, in autopsy and biopsy tissue from human CNS primary demyelinating diseases, including MS (20 cases), idiopathic monophasic CNS demyelinating disease (Mdemy, four cases) and metabolic or immunopathological demyelinating disease (two cases). For comparison, tissues from CNS viral disease in which demyelination is a major feature (nine cases) were examined in the same way. Control CNS tissues (nine cases) from a range of other neurological and non-neurological diseases were also examined. Outside the MS and Mdemy groups, morphological evidence of virus associations with the BBB were found only in the acute and subacute viral encephalitides (three cases subacute sclerosing panencephalitis, one case of Herpes encephalitis) and in one case of disseminated Cytomegalovirus infection. In a small proportion of MS and Mdemy cases, particles resembling either adenovirus (one case of MS) or paramyxovirus (one case of MS, one case of Mdemy) were found in the vicinity of microvessels. In each case a different cell type or extracellular compartment was involved and an exact correlation between the virus particles and the demyelinating lesions could not be demonstrated. Furthermore, corroborative clinical or laboratory evidence of current CNS infection in these primary demyelinating disease cases was available only from the single positive Mdemy case and not from the two cases of MS. This and other previously published evidence from MS (which implicated a Coronavirus) and other diseases highlights the potential vulnerability to viral infection of cells associated with the BBB. Furthermore it is concluded that the detection rate of such infections in pathological tissue could underestimate their true frequency. A possible role of transient virus-BBB interactions in triggering focal inflammation, BBB breakdown and demyelination in some cases of MS and parainfectious demyelinating disease cannot be discounted.

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Tsymbaliuk, V., V. Semenova, L. Pichkur, O. Velychko, and D. Egorova. "Cellular and molecular mechanisms of the demyelination in the central nervous system and cell therapy approaches." Cell and Organ Transplantology 5, no. 1 (May 31, 2017): 74–78. http://dx.doi.org/10.22494/cot.v5i1.70.

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The review summarizes the current concepts of cell-tissue and molecular features of development of demyelinating processes in the central nervous system related to multiple sclerosis and its animal model – allergic encephalomyelitis. An analysis of recently published studies of this pathology, carried out with light and electron microscopy and immunohistochemical and molecular genetic methods, is given. New methodological approaches to the study of the pathomorhological aspects of demyelinating disorders allowed receiving in-depth understanding of the etiology and mechanisms of demyelination processes in the brain and spinal cord tissues at the cellular level and identifying the ways to develop effective modern methods of pathogenetic treatment of these diseases using cell therapy.

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Belov, S. E., and A. N. Boyko. "The central vein sign in the differential diagnosis of multiple sclerosis." Neurology, Neuropsychiatry, Psychosomatics 12, no. 1S (August 5, 2020): 29–32. http://dx.doi.org/10.14412/2074-2711-2020-1s-29-32.

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The current diagnosis of multiple sclerosis (MS) is based on confirmation of the disseminated pathological process in space and time in accordance with the McDonald criteria. Despite this, the search continues for specific markers of the disease, including those detected using neuroimaging techniques that have high sensitivity and specificity in the diagnosis of MS.The paper considers the central vein sign, a new promising diagnostic one of MS. This sign refers to a parenchymal vein visualized in the focus of demyelination, by using special magnetic resonance imaging (MRI) modes. Studies show that the central vein sign has high sensitivity and specificity in the diagnosis of MS, allowing it to be differentiated from other demyelinating, vascular, and systemic diseases that have an MRI pattern similar to that of MS. According to various authors, a threshold of 40–50% perivenular lesions allows MS and MS-like diseases to be differentiated with high accuracy.

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Jeppesen, Rose, Christoffer Frederik Bang Jensen, Michael Stormly Hansen, and Shanu Faerch Roemer. "Illicit Sympathomimetic Drug Abuse in Demyelinating Diseases." Annals of Behavioral Neuroscience 1, no. 1 (May 7, 2018): 14–20. http://dx.doi.org/10.18314/abne.v1i1.1049.

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Multiple Sclerosis (MS) is an inflammatory demyelinating disease characterized by progressive motor deficits. Behavioral problems have previously been linked to the use of illicit drugs such as cocaine and amphetamine. We present 4 patients with frequent abuse of illicit sympathomimetics who presented with symptomatic White Matter Lesions (WML). Three patients had positive Oligoclonal Bands (OCB), one patient without OCB revealed marked pleocytosis. In this case-series we present clinical and radiological features and discuss possible mechanisms underlying substance abuse in patients with demyelinating lesions. Previous case reports in illicit sympathomimetic substance abusers highlight leukoencephalopathy rather than focally demyelinating WML. We hypothesize a two hit model with drug abuse exacerbating an unknown underlying diagnosis of MS.

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Curcio, Angela M., Jennifer M. Bain, Erin S. Beck, and Wendy S. Vargas. "Pediatric Inflammatory and Autoimmune Neurologic Disorders at a Tertiary Medical Center." Journal of Child Neurology 35, no. 14 (July 17, 2020): 949–52. http://dx.doi.org/10.1177/0883073820941751.

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Objectives: To describe the spectrum of pediatric inflammatory neurologic diseases and compare the sensitivity of ancillary testing for these diagnoses. Methods: We analyzed clinical features and outcomes of 98 children with an immune-mediated central nervous system disorder. We compared sensitivities of each diagnostic modality. Results: We identified the following diagnoses: acute cerebellar ataxia (n = 14; 14.3%), acute demyelinating encephalomyelitis (n = 13; 13.3%), multiple sclerosis (MS) (n = 18; 18.4%), anti- N-methyl-d-aspartate receptor encephalitis (anti-NMDAR encephalitis) (n = 15; 15.3%), encephalitis not otherwise specified (n = 12; 12.2%), and “Other” (n = 26; 26.5%). “Other” included acute transverse myelitis, neuromyelitis optica, central nervous system lupus, primary central nervous system vasculitis, Rasmussen encephalitis, opsoclonus myoclonus ataxia syndrome, and clinically isolated syndrome. The mean age of onset of all diagnoses was 7.9 ± 5.5 years. The diagnostic sensitivity of magnetic resonance imaging (MRI) for acute demyelinating encephalomyelitis and multiple sclerosis was 92.3% and 94.4%, respectively. Cerebrospinal fluid was sensitive for multiple sclerosis in 92.3%, where 75% of patients had cerebrospinal fluid oligoclonal bands. Electroencephalogram (EEG) coupled with cerebrospinal fluid studies was highly sensitive for anti-NMDAR encephalitis (100%). EEG was sensitive for acute demyelinating encephalomyelitis and encephalitis not otherwise specified (77.8% and 80%). No diagnostic studies were sensitive for acute cerebellar ataxia. Seventy-three percent of patients with multiple sclerosis had residual deficits. Thirty-six percent of anti-NMDAR encephalitis patients were nonverbal and wheel-chair bound. Conclusions: We found that MRI is useful for detecting multiple sclerosis and acute demyelinating encephalomyelitis, cerebrospinal fluid is helpful in diagnosing multiple sclerosis and anti-NMDAR encephalitis, and EEG is often abnormal in suspected anti-NMDAR encephalitis, acute demyelinating encephalomyelitis, and encephalitis not otherwise specified. Neurologic outcome at follow-up was unfavorable in patients with multiple sclerosis and anti-NMDAR encephalitis.

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Mastronardi, FG, H. Tsui, S. Winer, DD Wood, T. Selvanantham, C. Galligan, EN Fish, H.-M. Dosch, and MA Moscarello. "Synergy between paclitaxel plus an exogenous methyl donor in the suppression of murine demyelinating diseases." Multiple Sclerosis Journal 13, no. 5 (February 16, 2007): 596–609. http://dx.doi.org/10.1177/1352458506072167.

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Progressive demyelination in multiple sclerosis (MS) reflects the negative balance between myelin damage and repair due to physical and molecular barriers, such as astrocytic glial scars, between oligodendrocytes and target neurons. In this paper, we show that combination therapy with paclitaxel (Taxol®) plus the universal methyl-donor, vitamin B12CN (B12CN), dramatically limits progressive demyelination, and enhances remyelination in several independent, immune and nonimmune, in vivo and in vitro model systems. Combination therapy significantly reduced clinical signs of EAE in SJL mice, as well as the spontaneously demyelinating ND4 transgenic mouse. Astrocytosis was normalised in parallel to ultrastructural and biochemical evidence of remyelination. The combination therapy suppressed T cell expansion, reduced IFN-gamma, while enhancing IFN-beta and STAT-1 expression, STAT-1 phosphorylation and methylation of STAT-1 and MBP in the brain. Paclitaxel/B12CN has nearly identical effects to the previously described combination of IFN-beta/ B12CN, whose clinical usefulness is transient because of IFN-neutralising antibodies, not observed (or expected) with the present drug combination. This report provides a mechanistic foundation for the development of a new therapeutic strategy in humans with MS. Multiple Sclerosis 2007; 13: 596-609. http://msj.sagepub.com

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Bester, Maxim, Maria Petracca, and Matilde Inglese. "Neuroimaging of Multiple Sclerosis, Acute Disseminated Encephalomyelitis, and Other Demyelinating Diseases." Seminars in Roentgenology 49, no. 1 (January 2014): 76–85. http://dx.doi.org/10.1053/j.ro.2013.09.002.

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Kaya, Derya, Egemen İdiman, and Serkan Özakbaş. "Inflammatory Demyelinating Central Nervous System Diseases in Childhood: Clinical and Paraclinical Profiles in 133 Patients." Autoimmune Diseases 2012 (2012): 1–6. http://dx.doi.org/10.1155/2012/957802.

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In a retrospective review of patients with acquired demyelinating disorders of the central nervous system, 133 patients (5.6%) whose diseases started in childhood, were selected from 2369 patients, who had medical records in the Neurology Department of Dokuz Eylul University. Out of 133, 98 had relapsing remitting multiple sclerosis, 21 had secondary progressive multiple sclerosis, 8 had clinically isolated syndrome, 3 had neuromyelitis optica, 2 had Marburg disease, and 1 had radiologically isolated syndrome. In 55 patients (41.3%), disease onset was before age 16. Polysymptomatic presentation (22.6%) was the most common initial feature. The EDSS scores ranged from 0 to 9 with a median of 2.0 () for 126 patients. MRI records of 111 patients were obtained. 97 patients had clinically definite multiple sclerosis. 11 MS patients (11.3%) did not initially present the diagnostic MRI features. All of the remaining multiple sclerosis patients fulfilled Barkhof-Tintore criteria (100%) and 88.7% fulfilled KIDMUS criteria. Cranial MRI of NMO patients was normal. Our findings demonstrate some important clinical and paraclinical features that can help the literature on acquired demyelinating disorders of childhood by utilizing data from Western Turkey.

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Flores, Jose, Silvia González, Ximena Morales, Petra Yescas, Adriana Ochoa, and Teresa Corona. "Absence of Multiple Sclerosis and Demyelinating Diseases among Lacandonians, a Pure Amerindian Ethnic Group in Mexico." Multiple Sclerosis International 2012 (2012): 1–4. http://dx.doi.org/10.1155/2012/292631.

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Multiple Sclerosis (MS) is a highly polymorphic disease characterized by different neurologic signs and symptoms. In MS, racial and genetic factors may play an important role in the geographic distribution of this disease. Studies have reported the presence of several protective alleles against the development of autoimmune disorders. In the case of MS, however, they help define MS as a complex disease, and confirm the importance of environmental agents as an independent variable not associated with ethnicity. We carried out an on-site epidemiological study to confirm the absence of MS or NMO among Lacandonians, a pure Amerindian ethnic group in Mexico. We administered a structured interview to 5,372 Lacandonians to assess by family background any clinical data consistent with the presence of a prior demyelinating event. Every participating subject underwent a comprehensive neurological examination by a group of three members of the research team with experience in the diagnosis and treatment of demyelinating disorders to detect clinical signs compatible with a demyelinating disease. We did not find any clinical signs compatible with multiple sclerosis among study participants.

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Агафьина, А. С., А. Ю. Рудник, М. А. Федяков, О. С. Глотов, Т. Н. Кашко, Д. Г. Короткова, and Г. В. Буянова. "More on differential diagnosis of demyelinating and hereditary diseases." Nauchno-prakticheskii zhurnal «Medicinskaia genetika», no. 4(213) (April 30, 2020): 82–83. http://dx.doi.org/10.25557/2073-7998.2020.04.82-83.

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Демиелинизирующие заболевания являются гетерогенной группой, включающей рассеянный склероз (РС), острый рассеянный энцефаломиелит, оптиконевромиелит (ОНМ), идиопатический поперечный миелит, оптический неврит. Дифференциально-диагностический поиск при демиелинизирующих заболеваниях включает в себя в том числе и наследственные/нейродегенеративные заболевания. Сходство некоторых митохондриальных болезней (МБ) с РС не случайно, поскольку в настоящее время этиопатогенез РС рассматривается не только как аутоиммунная демиелинизация, но и как нейродегенерация, одним из важных патогенетических механизмов которой является митохондриальная дисфункция. В статье проведен краткий анализ пациентов с нарушением зрительных функций и нетипичной для РС клинической картиной. Критерием отбора больных был первичный клинический эпизод, вызванный предположительно воспалительным демиелинизирующим процессом и жалобами на снижение зрительных функций. Demyelinating diseases are heterogeneous group including multiple sclerosis (MS), acute multiple encephalomyelitis, opticoneuromyelitis (ONM), idiopathic transverse myelitis, optical neuritis. The spectrum of differential diagnostic screening in this rare autoimmune disease is variable, including hereditary/neurodegenerative diseases. The similarity of some mitochondrial diseases (MD) with MS is not accidental, since currently etiopathogenesis of MS is considered not only as autoimmune demyelination, but also as neurodegeneration, one of the important pathogenetic mechanisms of which is mitochondrial dysfunction. The article provides a brief analysis of patients with impaired visual functions and atypical clinical-diagnostic picture for MS. The selection criterion for patients was a primary clinical episode caused by a presumably inflammatory demyelinating process and complaints of decreased visual functions.

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

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