Multiple sclerosis New Drugs Review
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Cryopreserved vitamin D 3 -tolerogenic dendritic cells pulsed with autoantigens as a potential therapy for multiple sclerosis patients

Cryopreserved vitamin D 3 -tolerogenic dendritic cells pulsed with autoantigens as a potential therapy for multiple sclerosis patients | Multiple sclerosis New Drugs Review | Scoop.it
Tolerogenic dendritic cells (tolDC) have been postulated as a potent immunoregulatory therapy for autoimmune diseases such as multiple sclerosis (MS). In a previous study, we demonstrated that the administration of antigen-specific vitamin D3 (vitD3) tolDC in mice showing clinical signs of experimental autoimmune encephalomyelitis (EAE; the animal model of MS) resulted in abrogation of disease progression. With the purpose to translate this beneficial therapy to the clinics, we have investigated the effectivity of vitD3-frozen antigen-specific tolDC pulsed with myelin oligodendrocyte glycoprotein 40-55 peptide (f-tolDC-MOG) since it would reduce the cost, functional variability and number of leukapheresis to perform to the patients. Mice showing EAE clinical signs were treated with repetitive doses of f-tolDC-MOG. Tolerogenic mechanisms induced by the therapy were analysed by flow cytometry and T cell proliferation assays. Treatment with f-tolDC-MOG was effective in ameliorating clinical signs of mice with EAE, inhibiting antigen-specific reactivity and inducing Treg. In addition, the long-term treatment was well tolerated and leading to a prolonged maintenance of tolerogenicity mediated by induction of Breg, reduction of NK cells and activation of immunoregulatory NKT cells. The outcomes of this study show that the use of antigen-specific f-tolDC promotes multiple and potent tolerogenic mechanisms. Moreover, these cells can be kept frozen maintaining their tolerogenic properties, which is a relevant step for their translation to the clinic. Altogether, vitD3 f-tolDC-MOG is a potential strategy to arrest the autoimmune destruction in MS patients.
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Daclizumab (Biogen, Abbott) Review: Multiple sclerosis - Krishan Maggon

Daclizumab (Biogen, Abbott) Review: Multiple sclerosis - Krishan Maggon | Multiple sclerosis New Drugs Review | Scoop.it
Daclizumab is a humanized monoclonal antibody which targets the CD25 alpha subunit of the high affinity receptor and inhibits...
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Association of Rituximab Treatment with Disability Progression Among Patients with Secondary Progressive Multiple Sclerosis

Association of Rituximab Treatment with Disability Progression Among Patients with Secondary Progressive Multiple Sclerosis | Multiple sclerosis New Drugs Review | Scoop.it
Secondary progressive multiple sclerosis (SPMS) is the second most common type of multiple sclerosis, a demyelinating syndrome of the central nervous system.
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Could a safer version of an old blood pressure drug be repurposed in multiple sclerosis? | FierceBiotech

Could a safer version of an old blood pressure drug be repurposed in multiple sclerosis? | FierceBiotech | Multiple sclerosis New Drugs Review | Scoop.it
In 2015, a team of scientists at the University of Chicago found that the hypertension drug Wytensin could protect myelin in animal models of multiple sclerosis. Now, they've returned with data showing a similar drug could serve as a safer alternative.
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Comparison of fingolimod, dimethyl fumarate and teriflunomide for multiple sclerosis

Comparison of fingolimod, dimethyl fumarate and teriflunomide for multiple sclerosis | Multiple sclerosis New Drugs Review | Scoop.it
Conclusion The effect of fingolimod on relapse frequency was superior to teriflunomide and dimethyl fumarate. The effect of the three oral therapies on disability outcomes was similar during the initial 2.5 years on treatment. Persistence on fingolimod was superior to the two comparator drugs.

http://dx.doi.org/10.1136/jnnp-2018-319831
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Protecting oligodendrocytes may reduce the impact of multiple sclerosis

Protecting oligodendrocytes may reduce the impact of multiple sclerosis | Multiple sclerosis New Drugs Review | Scoop.it
A small molecule, Sephin1, may be able to significantly delay harm to nerve cells caused by multiple sclerosis, a disabling immune-mediated disease that damages nerve fibers in the brain and spinal cord.
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Cells | Ocrelizumab Depletes CD20+ T Cells in Multiple Sclerosis Patients | HTML

Cells | Ocrelizumab Depletes CD20+ T Cells in Multiple Sclerosis Patients | HTML | Multiple sclerosis New Drugs Review | Scoop.it
Ocrelizumab, a humanized monoclonal anti-CD20 antibody, has shown pronounced effects in reduction of disease activity in multiple sclerosis (MS) patients and has recently been approved for the treatment of patients with relapsing MS (RMS) and primary progressive MS (PPMS).
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B cell depletion in the treatment of multiple sclerosis: Expert Opinion on Biological Therapy: Vol 0, No ja

B cell depletion in the treatment of multiple sclerosis: Expert Opinion on Biological Therapy: Vol 0, No ja | Multiple sclerosis New Drugs Review | Scoop.it
ABSTRACT
Introduction: Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system. The latest development of B-cell depletion by anti-CD20 monoclonal antibodies has been a large step forward in the treatment of this devastating disease.

Areas covered: In this manuscript, we review mechanisms of action, efficacy, safety and tolerance of anti-CD20 therapies for MS, including rituximab, ocrelizumab, and ofatumumab.

Expert Opinion: B-cell depletion efficiently suppresses acute inflammatory disease activity in relapsing-remitting MS (RRMS), and may slow down progression in primary progressive MS (PPMS). The treatment is generally well tolerated, with manageable adverse events related to infusion reactions and infections. Ocrelizumab, a humanized anti-CD20 monoclonal antibody, is the first therapy to be approved for the treatment of both RRMS and PPMS.

Keywords: Multiple sclerosis, B cell, anti-CD20 antibody, rituximab, ocrelizumab, ofatumumab, treatment
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Fingolimod: Lessons Learned and New Opportunities for Treating Multiple Sclerosis and Other Disorders | Annual Review of Pharmacology and Toxicology

Fingolimod: Lessons Learned and New Opportunities for Treating Multiple Sclerosis and Other Disorders | Annual Review of Pharmacology and Toxicology | Multiple sclerosis New Drugs Review | Scoop.it
Abstract
Fingolimod (FTY720, Gilenya) was the first US Food and Drug Administration–approved oral therapy for relapsing forms of multiple sclerosis (MS). Research on modified fungal metabolites converged with basic science studies that had identified lysophospholipid (LP) sphingosine 1-phosphate (S1P) receptors, providing mechanistic insights on fingolimod while validating LP receptors as drug targets. Mechanism of action (MOA) studies identified receptor-mediated processes involving the immune system and the central nervous system (CNS). These dual actions represent a more general theme for S1P and likely other LP receptor modulators. Fingolimod's direct CNS activities likely contribute to its efficacy in MS, with particular relevance to treating progressive disease stages and forms that involve neurodegeneration. The evolving understanding of fingolimod's MOA has provided strategies for developing next-generation compounds with superior attributes, suggesting new ways to target S1P as well as other LP receptor modulators for novel therapeutics in the CNS and other organ systems.

Keywords
GPCRs, lysophospholipids, LPA, S1P, FTY720, Gilenya, neurodegeneration, drugs, medicines
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Distinct patterns of glia repair and remyelination in antibody‐mediated demyelination models of multiple sclerosis and neuromyelitis optica - Liu - 2018 - Glia - Wiley Online Library

Distinct patterns of glia repair and remyelination in antibody‐mediated demyelination models of multiple sclerosis and neuromyelitis optica - Liu - 2018 - Glia - Wiley Online Library | Multiple sclerosis New Drugs Review | Scoop.it
Multiple sclerosis (MS) and neuromyelitis optica (NMO) are inflammatory demyelinating disorders of the central nervous system with evidence of antibody‐mediated pathology. Using ex vivo organotypic mouse cerebellar slice cultures, we have demonstrated that recombinant antibodies (rAbs) cloned from cerebrospinal fluid plasmablasts of MS and NMO patients target myelin‐ and astrocyte‐specific antigens to induce disease‐specific oligodendrocyte loss and myelin degradation. In this study, we examined glial cell responses and myelin integrity during recovery from disease‐specific antibody‐mediated injury. Following exposure to MS rAb and human complement (HC) in cerebellar explants, myelinating oligodendrocytes repopulated the demyelinated tissue and formed new myelin sheaths along axons. Remyelination was accompanied by pronounced microglial activation. In contrast, following treatment with NMO rAb and HC, there was rapid regeneration of astrocytes and pre‐myelinating oligodendrocytes but little formation of myelin sheaths on preserved axons. Deficient remyelination was associated with progressive axonal loss and the return of microglia to a resting state. Our results indicate that antibody‐mediated demyelination in MS and NMO show distinct capacities for recovery associated with differential injury to adjacent axons and variable activation of microglia. Remyelination was rapid in MS rAb plus HC‐induced demyelination. By contrast, oligodendrocyte maturation and remyelination failed following NMO rAb‐mediated injury despite the rapid restoration of astrocytes and preservation of axons in early lesions.
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Managing Risks with Immune Therapies in Multiple Sclerosis

Managing Risks with Immune Therapies in Multiple Sclerosis | Multiple sclerosis New Drugs Review | Scoop.it
Abstract
Since the introduction of the interferons in the 1990s, a multitude of different immunomodulatory and immunosuppressant disease-modifying therapies for multiple sclerosis (MS) have been developed. They have all shown positive effects on clinical endpoints such as relapse rate and disease progression and are a heterogeneous group of therapeutics comprising recombinant pegylated and non-pegylated interferon-β variants, peptide combinations, monoclonal antibodies, and small molecules. However, they have relevant side effect profiles, which necessitate thorough monitoring and straightforward patient education. In individual cases, side effects can be severe and potentially life-threatening, which is why knowledge about (neurological and non-neurological) adverse drug reactions is essential for prescribing neurologists as well as general practitioners. This paper aims to provide an overview of currently available MS therapies, their modes of action and safety profiles, and the necessary therapy monitoring.
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Immune cells from the gut found to reduce MS-related brain inflammation

Immune cells from the gut found to reduce MS-related brain inflammation | Multiple sclerosis New Drugs Review | Scoop.it
An incredible new study has provided a novel insight into the gut-brain connection, revealing the intestine may be the source of immune cells found to reduce brain inflammation in multiple sclerosis (MS) sufferers.
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Immunology and Oxidative Stress in Multiple Sclerosis: Clinical and Basic Approach

Immunology and Oxidative Stress in Multiple Sclerosis: Clinical and Basic Approach | Multiple sclerosis New Drugs Review | Scoop.it
Multiple sclerosis (MS) exhibits many of the hallmarks of an inflammatory autoimmune disorder including breakdown of the
blood-brain barrier (BBB), the recruitment of lymphocytes, microglia, and macrophages to lesion sites, the presence of multiple lesions, ...
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Novel prognostic predictor of brain atrophy in multiple sclerosis

Novel prognostic predictor of brain atrophy in multiple sclerosis | Multiple sclerosis New Drugs Review | Scoop.it
Cognitive impairment occurs in more than half of patients with multiple sclerosis (MS) and is a leading cause of disability.1 The Paced Auditory Serial Addition Test (PASAT) is part of the Multiple Sclerosis Functional Composite (MSFC) and has been widely used in clinical research to assess...
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Brain and cord imaging features in neuromyelitis optica spectrum disorders - Cacciaguerra - - Annals of Neurology - Wiley Online Library

Brain and cord imaging features in neuromyelitis optica spectrum disorders - Cacciaguerra - - Annals of Neurology - Wiley Online Library | Multiple sclerosis New Drugs Review | Scoop.it
Objectives To validate imaging features able to discriminate neuromyelitis optica spectrum disorders from multiple sclerosis with conventional MRI. Methods In this cross‐sectional study, brain and spinal cord scans were evaluated from 116 neuromyelitis optica spectrum disorders patients (98 seropositive and 18 seronegative) in chronic disease phase and 65 age‐, sex‐ and disease duration‐matched multiple sclerosis patients. To identify independent predictors of neuromyelitis optica diagnosis, after assessing the prevalence of typical/atypical findings, the original cohort was 2:1 randomized in a training sample (where a multivariate logistic regression analysis was run) and a validation sample (where the performance of the selected variables was tested and validated). Results Typical brain lesions occurred in 50.9% of neuromyelitis optica patients (18.1% brainstem periventricular/periaqueductal; 32.7% periependymal along lateral ventricles, 3.4% large hemispheric; 6.0% diencephalic; 4.3% cortico‐spinal tract), 72.2% had spinal cord lesions (46.3% long transverse myelitis, 36.1% short transverse myelitis) 37.1% satisfied 2010 McDonald criteria and none had cortical lesions. Fulfillment of at least 2/5 of: absence of juxtacortical/cortical lesions, absence of periventricular lesions, absence of Dawson's fingers, presence of long transverse myelitis or presence of periependymal lesions along lateral ventricles, discriminated neuromyelitis optica patients in both training (sensitivity [95% confidence interval ]=0.92 [0.84‐0.97], specificity=0.91 [0.78‐0.97]) and validation samples (sensitivity=0.82 [0.66‐0.92], specificity=0.91 [0.71‐0.99]). MRI findings and criteria performance were similar irrespective of serostatus. Interpretation Although up to 50% of neuromyelitis optica patients have no typical lesions and a relatively high percentage of them satisfies multiple sclerosis criteria, several easily applicable imaging features can help to identify neuromyelitis optica from multiple sclerosis. This article is protected by copyright. All rights reserved.
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Obesity and Multiple Sclerosis Susceptibility: A Review | Journal of Neurology & Neuromedicine

Obesity and Multiple Sclerosis Susceptibility: A Review | Journal of Neurology & Neuromedicine | Multiple sclerosis New Drugs Review | Scoop.it
 Several studies conducted around the world over the last decade...
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Association of Initial Disease-Modifying Therapy With Later Conversion to Secondary Progressive Multiple Sclerosis. | Demyelinating Disorders | JAMA | JAMA Network

Association of Initial Disease-Modifying Therapy With Later Conversion to Secondary Progressive Multiple Sclerosis. | Demyelinating Disorders | JAMA | JAMA Network | Multiple sclerosis New Drugs Review | Scoop.it
In this cohort study, initial treatment of patients with relapsing-remitting multiple sclerosis (MS) with disease-modifying therapies (fingolimod, natalizumab, or alemtuzumab) was associated with a lower risk of conversion to secondary progressive MS compared with interferon beta o
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Quantitative neuroimaging measures of myelin in the healthy brain and in multiple sclerosis - O'Muircheartaigh - - Human Brain Mapping - Wiley Online Library

Abstract
Quantitative magnetic resonance imaging (MRI) techniques have been developed as imaging biomarkers, aiming to improve the specificity of MRI to underlying pathology compared to conventional weighted MRI. For assessing the integrity of white matter (WM), myelin, in particular, several techniques have been proposed and investigated individually. However, comparisons between these methods are lacking. In this study, we compared four established myelin‐sensitive MRI techniques in 56 patients with relapsing–remitting multiple sclerosis (MS) and 38 healthy controls. We used T2‐relaxation with combined GRadient And Spin Echoes (GRASE) to measure myelin water fraction (MWF‐G), multi‐component driven equilibrium single pulse observation of T1 and T2 (mcDESPOT) to measure MWF‐D, magnetization‐transfer imaging to measure magnetization‐transfer ratio (MTR), and T1 relaxation to measure quantitative T1 (qT1). Using voxelwise Spearman correlations, we tested the correspondence of methods throughout the brain. All four methods showed associations that varied across tissue types; the highest correlations were found between MWF‐D and qT1 (median ρ across tissue classes 0.8) and MWF‐G and MWF‐D (median ρ = 0.59). In eight WM tracts, all measures showed differences (p < 0.05) between MS normal‐appearing WM and healthy control WM, with qT1 showing the highest number of different regions (8), followed by MWF‐D and MTR (6), and MWF‐G (n = 4). Comparing the methods in terms of their statistical sensitivity to MS lesions in WM, MWF‐D demonstrated the best accuracy (p < 0.05, after multiple comparison correction). To aid future power analysis, we provide the average and standard deviation volumes of the four techniques, estimated from the healthy control sample.
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Unraveling the mysteries of multiple sclerosis

Unraveling the mysteries of multiple sclerosis | Multiple sclerosis New Drugs Review | Scoop.it
Leiden chemists discovered a new mechanism which might explain how multiple sclerosis shifts to a more severe form. Their findings contribute to unraveling the mysterious course of the disease. They have published their findings ...
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The topographical model of multiple sclerosis

The topographical model of multiple sclerosis | Multiple sclerosis New Drugs Review | Scoop.it
Relapses and progression contribute to multiple sclerosis (MS) disease course, but neither the relationship between them nor the spectrum of clinical heterogeneity has been fully characterized. A hypothesis-driven, biologically informed model could build ...
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Can Viruses in the Genome Cause Disease?

Can Viruses in the Genome Cause Disease? | Multiple sclerosis New Drugs Review | Scoop.it
Clinical trials that target human endogenous retroviruses to treat multiple sclerosis, ALS, and other ailments are underway, but many questions remain about how these sequences may disrupt our biology.
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Increased mRNA expression of IL-23 in the peripheral blood of patients with multiple sclerosis | JNEUROLOGY

Increased mRNA expression of IL-23 in the peripheral blood of patients with multiple sclerosis | JNEUROLOGY | Multiple sclerosis New Drugs Review | Scoop.it
Increased mRNA expression of IL-23 in the peripheral blood of patients with multiple sclerosis, Journal of Immunological Sciences...
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Practice guideline recommendations summary: Disease-modifying therapies for adults with multiple sclerosis: Report of the Guideline Development, Dissemination, and Implementation Subcommittee of th...

Practice guideline recommendations summary: Disease-modifying therapies for adults with multiple sclerosis: Report of the Guideline Development, Dissemination, and Implementation Subcommittee of th... | Multiple sclerosis New Drugs Review | Scoop.it
Latest Medical News & Articles...
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Monoclonal Antibodies for Multiple Sclerosis: An Update

Monoclonal Antibodies for Multiple Sclerosis: An Update | Multiple sclerosis New Drugs Review | Scoop.it
The use of monoclonal antibodies in multiple sclerosis (MS) patients is in a transitional period. Studies regarding well-established, effective antibodies such as natalizumab and alemtuzuma
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Tysabri – How It Works To Fight Multiple Sclerosis – Patient Talk

Tysabri – How It Works To Fight Multiple Sclerosis – Patient Talk | Multiple sclerosis New Drugs Review | Scoop.it
This is a short 3 minute video that explains how Tysabri works, it’s excellent.
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Meningeal inflammation and cortical demyelination in acute multiple sclerosis - Bevan - 2018 - Annals of Neurology - Wiley Online Library

Objective Cortical gray matter (GM) pathology, involving demyelination and neurodegeneration, associated with meningeal inflammation, could be important in determining disability progression in multiple sclerosis (MS). However, we need to know more about how cortical demyelination, neurodegeneration, and meningeal inflammation contribute to pathology at early stages of MS to better predict long‐term outcome. Methods Tissue blocks from short disease duration MS (n = 12, median disease duration = 2 years), progressive MS (n = 21, disease duration = 25 years), non‐diseased controls (n = 11), and other neurological inflammatory disease controls (n = 6) were quantitatively analyzed by immunohistochemistry, immunofluorescence, and in situ hybridization. Results Cortical GM demyelination was extensive in some cases of acute MS (range = 1–48% of total cortical GM), and subpial lesions were the most common type (62%). The numbers of activated (CD68+) microglia/macrophages were increased in cases with subpial lesions, and the density of neurons was significantly reduced in acute MS normal appearing and lesion GM, compared to controls (p < 0.005). Significant meningeal inflammation and lymphoid‐like structures were seen in 4 of 12 acute MS cases. The extent of meningeal inflammation correlated with microglial/macrophage activation (p < 0.05), but not the area of cortical demyelination, reflecting the finding that lymphoid‐like structures were seen adjacent to GM lesions as well as areas of partially demyelinated/remyelinated, cortical GM. Interpretation Our findings demonstrate that cortical demyelination, neuronal loss, and meningeal inflammation are notable pathological hallmarks of acute MS and support the need to identify early biomarkers of this pathology to better predict outcome. Ann Neurol 2018;84:829–842
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Monitoring Progressive Multiple Sclerosis with Novel Imaging Techniques - Europe PMC Article - Europe PMC

Monitoring Progressive Multiple Sclerosis with Novel Imaging Techniques - Europe PMC Article - Europe PMC | Multiple sclerosis New Drugs Review | Scoop.it
Imaging markers for monitoring disease progression in progressive multiple sclerosis (PMS) are scarce, thereby limiting the possibility to monitor disease evolution and to test effective treatments in clinical trials.
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