scholarly journals Beneficial contribution of iPSC-progeny to connexin 47 dynamics during demyelination-remyelination

2020 ◽  
Author(s):  
Sabah Mozafari ◽  
Cyrille Deboux ◽  
Cecilia Laterza ◽  
Marc Ehrlich ◽  
Tanja Kuhlmann ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Cell Therapy ◽  
Demyelinating Diseases ◽  
Neural Precursors ◽  
Myelin Disorders

AbstractOligodendrocytes are extensively coupled to astrocytes, a phenomenon ensuring glial homeostasis and maintenance of CNS myelin. Molecular disruption of this communication occurs in demyelinating diseases such as multiple sclerosis. Less is known about the vulnerability and reconstruction of the panglial network during adult demyelination-remyelination. Here, we took advantage of LPC-induced demyelination to investigate the expression dynamics of the oligodendrocyte specific connexin 47 (Cx47) and whether this dynamic could be modulated by grafted iPSC-neural progeny. Our data show that deconstruction of the panglial network following demyelination is larger in size than demyelination. Loss of Cx47 expression is timely rescued during remyelination and accelerated by the grafted neural precursors. Moreover, mouse and human iPS-derived oligodendrocytes express Cx47, which co-labels with astrocyte Cx43, indicating their integration into the panglial network. These data suggest that full lesion repair following transplantation occurs by panglial reconstruction in addition to remyelination. Targeting panglial elements by cell therapy or pharmacological compounds may help accelerating or stabilizing re/myelination in myelin disorders.

The role of SVZ-derived neural precursors in demyelinating diseases: From animal models to multiple sclerosis

2008 ◽  
Vol 265 (1-2) ◽  
pp. 26-31 ◽  
Author(s):  
B. Nait-Oumesmar ◽  
Nathalie Picard-Riéra ◽  
Christophe Kerninon ◽  
A. Baron-Van Evercooren
Keyword(s):  
Multiple Sclerosis ◽  
Animal Models ◽  
Demyelinating Diseases ◽  
Neural Precursors

scholarly journals Five Decades of Cuprizone, an Updated Model to Replicate Demyelinating Diseases

2019 ◽  
Vol 17 (2) ◽  
pp. 129-141 ◽  
Author(s):  
Jose M. Vega-Riquer ◽  
Gerardo Mendez-Victoriano ◽  
Raul A. Morales-Luckie ◽  
Oscar Gonzalez-Perez
Keyword(s):  
Multiple Sclerosis ◽  
Clinical Signs ◽  
Behavioral Changes ◽  
Demyelinating Diseases ◽  
Histological Changes ◽  
Cerebellar Peduncles ◽  
The Central Nervous System ◽  
Myelin Disorders ◽  
The Brain ◽  
Pharmacological Model

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.

scholarly journals Ultra-high-field 7-T MRI in multiple sclerosis and other demyelinating diseases: from pathology to clinical practice

2020 ◽  
Vol 4 (1) ◽  
Author(s):  
Nicolo’ Bruschi ◽  
Giacomo Boffa ◽  
Matilde Inglese
Keyword(s):  
Multiple Sclerosis ◽  
High Field ◽  
Neurological Diseases ◽  
Lesion Detection ◽  
Demyelinating Diseases ◽  
Metabolic Imaging ◽  
Central Vein ◽  
Ultra High Field ◽  
Functional Features

Abstract Magnetic resonance imaging (MRI) is essential for the early diagnosis of multiple sclerosis (MS), for investigating the disease pathophysiology, and for discriminating MS from other neurological diseases. Ultra-high-field strength (7-T) MRI provides a new tool for studying MS and other demyelinating diseases both in research and in clinical settings. We present an overview of 7-T MRI application in MS focusing on increased sensitivity and specificity for lesion detection and characterisation in the brain and spinal cord, central vein sign identification, and leptomeningeal enhancement detection. We also discuss the role of 7-T MRI in improving our understanding of MS pathophysiology with the aid of metabolic imaging. In addition, we present 7-T MRI applications in other demyelinating diseases. 7-T MRI allows better detection of the anatomical, pathological, and functional features of MS, thus improving our understanding of MS pathology in vivo. 7-T MRI also represents a potential tool for earlier and more accurate diagnosis.

Gene and cell therapy and nanomedicine for the treatment of multiple sclerosis: bibliometric analysis and systematic review of clinical outcomes

2021 ◽  
pp. 1-11
Author(s):  
Javier Caballero-Villarraso ◽  
Jamil Sawas ◽  
Begoña M. Escribano ◽  
Francisco A. Martín-Hersog ◽  
Andrea Valverde-Martínez ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Systematic Review ◽  
Cell Therapy ◽  
Clinical Outcomes ◽  
Bibliometric Analysis ◽  
Gene And Cell Therapy

scholarly journals Multiple Sclerosis in Malaysia: Demographics, Clinical Features, and Neuroimaging Characteristics

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
S. Viswanathan ◽  
N. Rose ◽  
A. Masita ◽  
J. S. Dhaliwal ◽  
S. D. Puvanarajah ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Neuromyelitis Optica ◽  
Demyelinating Disease ◽  
Age At Onset ◽  
Positive Family History ◽  
Disease Onset ◽  
Demyelinating Diseases ◽  
Lesion Length ◽  
Relapsing Remitting ◽  
Spectrum Disorders

Background. Multiple sclerosis (MS) is an uncommon disease in multiracial Malaysia. Diagnosing patients with idiopathic inflammatory demyelinating diseases has been greatly aided by the evolution in diagnostic criterion, the identification of new biomarkers, and improved accessibility to neuroimaging in the country.Objectives. To investigate the spectrum of multiple sclerosis in Malaysia.Methods. Retrospective analysis with longitudinal follow-up of patients referred to a single tertiary medical center with neurology services in Malaysia.Results. Out of 245 patients with idiopathic inflammatory demyelinating disease, 104 patients had multiple sclerosis. Female to male ratio was 5 : 1. Mean age at onset was 28.6 ± 9.9 years. The Malays were the predominant racial group affected followed by the Chinese, Indians, and other indigenous groups. Subgroup analysis revealed more Chinese having neuromyelitis optica and its spectrum disorders rather than multiple sclerosis. Positive family history was reported in 5%. Optic neuritis and myelitis were the commonest presentations at onset of disease, and relapsing remitting course was the commonest disease pattern observed. Oligoclonal band positivity was 57.6%. At disease onset, 61.5% and 66.4% fulfilled the 2005 and 2010 McDonald’s criteria for dissemination in space. Mean cord lesion length was 1.86 ± 1.65 vertebral segments in the relapsing remitting group as opposed to 6.25 ± 5.18 vertebral segments in patients with neuromyelitis optica and its spectrum disorders.Conclusion. The spectrum of multiple sclerosis in Malaysia has changed over the years. Further advancement in diagnostic criteria will no doubt continue to contribute to the evolution of this disease here.

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

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

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

Multiple Sclerosis and Related Disorders

2014 ◽  
Author(s):  
J William Lindsey
Keyword(s):  
Multiple Sclerosis ◽  
Differential Diagnosis ◽  
Neuromyelitis Optica ◽  
Subacute Sclerosing Panencephalitis ◽  
Large Diameter ◽  
Transverse Myelitis ◽  
Acute Disseminated Encephalomyelitis ◽  
Demyelinating Diseases ◽  
Pathologic Features ◽  
Relapsing Remitting

Multiple sclerosis (MS) is a relatively common cause of neurologic symptoms and disability in young adults. The distinguishing pathologic features of MS are loss of myelin and inflammation in the central nervous system (CNS). The myelin sheath is essential for rapid conduction of nerve signals along large-diameter axons. Oligodendrocytes produce and maintain myelin in the CNS, and Schwann cells produce and maintain myelin in the peripheral nerves. In addition to MS, there are a number of related disorders causing demyelination, inflammation, or both in the CNS. This chapter discusses MS and related disorders, including neuromyelitis optica, optic neuritis, acute disseminated encephalomyelitis, transverse myelitis, Behçet syndrome, neurosarcoidosis, inherited demyelinating diseases (leukodystrophies, cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy [CADASIL]), and virus-induced demyelination (progressive multifocal leukoencephalopathy, subacute sclerosing panencephalitis). The section on MS covers epidemiology, etiology/genetics, pathogenesis, diagnosis, differential diagnosis, management, and prognosis. Figures include organization of the microenvironment of larger-diameter axons, typical magnetic resonance imaging findings in MS and neuromyelitis optica, postgadolinium images of the cervical spine in MS, and an approach to treatment of relapsing-remitting MS. Tables list MS and related disorders, distribution of neurologic deficits at the onset of MS, differential diagnosis of MS, disease-modifying therapies for relapsing-remitting MS, and selected leukodystrophies, as well as diagnostic criteria and selected symptomatic therapies for MS. This review contains 3 highly rendered figures, 7 tables, and 82 references.

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