Database : MEDLINE
Search on : Multiple and Sclerosis [Words]
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[PMID]: 29524759
[Au] Autor:Cohan SL; Moses H; Calkwood J; Tornatore C; LaGanke C; Smoot KE; Meka V; Okwuokenye M; Hotermans C; Mendoza JP; Mann MK; Meltzer LA
[Ad] Address:Providence Multiple Sclerosis Center, Providence Health & Services, 9427 SW Barnes Road, Portland, OR 97225, USA; Providence Brain and Spine Institute, Providence Health & Services, 9135 SW Barnes Road, Suite 461, Portland, OR 97225, USA. Electronic address: stanley.cohan@providence.org.
[Ti] Title:Clinical outcomes in patients with relapsing-remitting multiple sclerosis who switch from natalizumab to delayed-release dimethyl fumarate: A multicenter retrospective observational study (STRATEGY).
[So] Source:Mult Scler Relat Disord;22:27-34, 2018 Feb 26.
[Is] ISSN:2211-0356
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:BACKGROUND: Delayed-release dimethyl fumarate (DMF) may be a therapeutic option for patients with relapsing-remitting multiple sclerosis (RRMS) who are treated with natalizumab and require a change in therapy. However, there is limited information regarding predictors of favorable treatment outcomes in patients switching from natalizumab to DMF. Clinical practices and sequencing protocols vary. Herein, we present the clinical results, including annualized relapse rate (ARR) and risk of relapse, of a phase 4 retrospective observational study of patients with RRMS who switched from natalizumab to DMF in a community practice setting (STRATEGY). METHODS: STRATEGY was performed through a single time point medical record abstraction; no study visits or procedures were required. Key inclusion criteria included age ≥ 18 years, RRMS diagnosis (McDonald criteria, 2010 revised), ≥ 12 months of continuous treatment with natalizumab monotherapy before DMF initiation, and initiation of DMF ≥ 12 months before enrollment. Patients were eligible to enroll regardless of current DMF use. RESULTS: A total of 530 patients at 45 US sites enrolled, and 506 met the inclusion criteria and were included in the modified evaluable population for analysis. Mean (SD) age at DMF initiation was 47.0 (10.9) years, with a mean (SD) of 12.7 (7.2) years since MS diagnosis. The mean (SD) duration of natalizumab treatment was 3.4 (1.9) years, and the mean (SD) washout from natalizumab discontinuation to DMF initiation (n = 502) was 101.6 (164.0) days. Overall risk of relapse 12 months after DMF initiation was 19.6%. Overall unadjusted ARR was higher during the 12 months following initiation of DMF treatment compared with the 12 months following initiation of natalizumab treatment (rate ratio, 2.32 [95% CI, 1.69-3.18]; p < 0.0001), but was lower compared with that observed in the year before initiation of natalizumab (rate ratio, 0.51 [95% CI, 0.40-0.64]; p < 0.0001). At 1 year following initiation of DMF treatment, the relapse rate was lower for patients who did not experience a relapse during 1 year following initiation of natalizumab treatment than for those who did (rate ratio for relapse rate, 0.47 [95% CI, 0.16-1.38]; p = 0.1664). The relapse rate for patients who did not relapse during natalizumab treatment was significantly lower with a washout period of ≤ 90 days as compared with a washout period of > 90 days (rate ratio for relapse rate, 0.49 [95% CI, 0.26-0.90]; p = 0.0216). A total of 42 (8%) patients reported ≥ 1 adverse event leading to DMF discontinuation during the study; the most commonly reported events were gastrointestinal disorders (n = 21; 4%). CONCLUSIONS: Results from this multicenter retrospective observational study suggest that DMF may be an effective treatment option for patients who discontinue natalizumab in routine clinical practice. ARR was lower in patients who initiated DMF within 90 days of natalizumab discontinuation compared with patients who initiated DMF after 90 days of natalizumab discontinuation. TRIAL REGISTRATION NUMBER: ClinicalTrials.gov identifier NCT02159573.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[Cl] Clinical Trial:ClinicalTrial
[St] Status:Publisher

  2 / 81752 MEDLINE  
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[PMID]: 29524760
[Au] Autor:Di Pauli F; Reindl M; Berger T
[Ad] Address:Clinical Department of Neurology, Medical University of Innsbruck, Anichstrasse 35, 6020 Innsbruck, Austria. Electronic address: franziska.dipauli@i-med.ac.at.
[Ti] Title:New clinical implications of anti-myelin oligodendrocyte glycoprotein antibodies in children with CNS demyelinating diseases.
[So] Source:Mult Scler Relat Disord;22:35-37, 2018 Feb 22.
[Is] ISSN:2211-0356
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Acquired demyelinating CNS syndromes include a broad spectrum of clinical phenotypes and different entities can overlap. Therefore, differential diagnosis is still challenging. A humoral immune reaction against myelin oligodendrocyte glycoprotein (MOG) is present in a subgroup of these patients, particularly in children. Anti-MOG antibodies indicate a non-multiple sclerosis disease course. Indeed, early publications have suggested that anti-MOG antibodies argue for a monophasic course; recently an association with a high risk for recurrent non-MS disease has been shown. According new data, antibody analysis was included in a diagnostic algorithm for the diagnosis of acquired demyelinating CNS syndromes in children. Here, recent data from the implementation of anti-MOG antibodies in daily clinical practice are reviewed.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  3 / 81752 MEDLINE  
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[PMID]: 29524758
[Au] Autor:Shahmohammadi S; Sahraian MA; Shahmohammadi A; Doosti R; Zare-Mirzaie A; Naser Moghadasi A
[Ad] Address:MS Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran.
[Ti] Title:A presentation of ulcerative colitis after rituximab therapy in a patient with multiple sclerosis and literature review.
[So] Source:Mult Scler Relat Disord;22:22-26, 2018 Mar 01.
[Is] ISSN:2211-0356
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Multiple sclerosis (MS) is one of the most important demyelinating diseases that affects the central nervous system. Its treatment often involves a long-term disease modifying therapy. According to some studies, the prevalence of autoimmune disorders, such as autoimmune hepatitis (AIH) and ulcerative colitis (UC) is higher in MS patients than in the normal population. There are also few studies that have reported the onset of UC after rituximab therapy. The present study presents a report of a 31-years old female patient suffering from aggressive multiple sclerosis, which developed into autoimmune hepatitis during the MS therapy. Thereafter, she received rituximab for the treating both MS and AIH. One week after the third cycle of rituximab (6 doses of 1000 mg), she experienced abdominal pain, fever, and severe bloody diarrhea; finally, she was diagnosed with ulcerative colitis (UC). It seems that the administration of certain immunomodulators or immunosuppressive drugs may have a main role in the exacerbation of some autoimmune diseases.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  4 / 81752 MEDLINE  
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[PMID]: 29524756
[Au] Autor:Swanberg KM; Prinsen H; Coman D; de Graaf RA; Juchem C
[Ad] Address:Department of Biomedical Engineering, Columbia University Fu Foundation School of Engineering and Applied Science, 1210 Amsterdam Ave., New York, NY 10027, United States; Department of Radiology and Biomedical Imaging, Yale University School of Medicine, 330 Cedar Street, New Haven, CT 06520, United
[Ti] Title:Quantification of glutathione transverse relaxation time T using echo time extension with variable refocusing selectivity and symmetry in the human brain at 7 Tesla.
[So] Source:J Magn Reson;290:1-11, 2018 Mar 01.
[Is] ISSN:1096-0856
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Glutathione (GSH) is an endogenous antioxidant implicated in numerous biological processes, including those associated with multiple sclerosis, aging, and cancer. Spectral editing techniques have greatly facilitated the acquisition of glutathione signal in living humans via proton magnetic resonance spectroscopy, but signal quantification at 7 Tesla is still hampered by uncertainty about the glutathione transverse decay rate T relative to those of commonly employed quantitative references like N-acetyl aspartate (NAA), total creatine, or water. While the T of uncoupled singlets can be derived in a straightforward manner from exponential signal decay as a function of echo time, similar estimation of signal decay in GSH is complicated by a spin system that involves both weak and strong J-couplings as well as resonances that overlap those of several other metabolites and macromolecules. Here, we extend a previously published method for quantifying the T of GABA, a weakly coupled system, to quantify T of the strongly coupled spin system glutathione in the human brain at 7 Tesla. Using full density matrix simulation of glutathione signal behavior, we selected an array of eight optimized echo times between 72 and 322 ms for glutathione signal acquisition by J-difference editing (JDE). We varied the selectivity and symmetry parameters of the inversion pulses used for echo time extension to further optimize the intensity, simplicity, and distinctiveness of glutathione signals at chosen echo times. Pairs of selective adiabatic inversion pulses replaced nonselective pulses at three extended echo times, and symmetry of the time intervals between the two extension pulses was adjusted at one extended echo time to compensate for J-modulation, thereby resulting in appreciable signal-to-noise ratio and quantifiable signal shapes at all measured points. Glutathione signal across all echo times fit smooth monoexponential curves over ten scans of occipital cortex voxels in nine subjects. The T of glutathione was calculated to be 145.0  20.1 ms (mean  standard deviation); this result was robust within one standard deviation to changes in metabolite fitting baseline corrections and removal of individual data points on the signal decay curve. The measured T of NAA (222.1  24.7 ms) and total creatine (153.0  19.9 ms) were both higher than that calculated for GSH. Apparent glutathione concentration quantified relative to both reference metabolites increased by up to 32% and 6%, respectively, upon correction with calculated T values, emphasizing the importance of considering T relaxation differences in the spectroscopic measurement of these metabolites, especially at longer echo times.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  5 / 81752 MEDLINE  
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[PMID]: 29524632
[Au] Autor:De Riccardis L; Buccolieri A; Muci M; Pitotti E; De Robertis F; Trianni G; Manno D; Maffia M
[Ad] Address:Department of Biological and Environmental Sciences and Technologies, University of Salento, via Monteroni, Lecce, Italy.
[Ti] Title:Copper and ceruloplasmin dyshomeostasis in serum and cerebrospinal fluid of multiple sclerosis subjects.
[So] Source:Biochim Biophys Acta;, 2018 Mar 07.
[Is] ISSN:0006-3002
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Although many studies have been carried out in order to understand the implication of copper (Cu) in the pathogenesis of multiple sclerosis (MS), the exact role that this metal plays in the disease is not still clear. Because of the lack of information in this subject, the present study compared the serum and cerebrospinal (CSF) levels of copper in MS patients in respect to a control group, matched for age and sex, finding a significant increase of metal concentrations, in both biological fluids of MS subjects. To confirm the possible impairment of Cu metabolism, we analyzed ceruloplasmin (Cp) level and activity, seeing as this protein is an established peripheral marker in diseases associated with Cu imbalance. By comparing these two parameters between control and MS subjects, we found an increase of Cp levels, associated with a decrease in Cp activity, in the second group. By analysing these data, free copper levels were calculated, significantly increased in serum of MS subjects; the increase in free copper could be one of the predisposing factors responsible for the Cu altered levels in CSF of MS patients. At the same time, this alteration could be attributable to the inability to incorporate Cu by Cp, probably due to the high oxidative environment found in serum of MS patients. Overall, all these copper alterations may play a role in MS pathogenesis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  6 / 81752 MEDLINE  
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[PMID]: 29517899
[Au] Autor:Mondal S; Parelkar SS; Nagar M; Thompson PR
[Ti] Title:Photochemical Control of Protein Arginine Deiminase (PAD) Activity.
[So] Source:ACS Chem Biol;, 2018 Mar 08.
[Is] ISSN:1554-8937
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Protein Arginine deiminases (PADs) play an important role in the pathogenesis of various diseases, including rheumatoid arthritis, multiple sclerosis, lupus, ulcerative colitis and breast cancer. Therefore, the development of PAD-inhibitors has drawn significant research interest in recent years. Herein, we describe the development of the first photoswitchable PAD-inhibitors. These compounds possess an azobenzene photoswitch to optically control PAD activity. Screening of a series of inhibitors structurally similar to BB-Cl-Amidine afforded compounds 1 and 2 as the most promising candidates for the light-controlled inhibition of PAD2; the cis-isomer of 1 is 10-fold more potent than its trans-isomer, whereas the trans-isomer of 2 is 45-fold more potent than the corresponding cis-isomer. The altered inhibitory potency upon photoisomerization has been confirmed in a competitive activity-based protein profiling (ABPP) assay. Further investigations indicate that the trans-isomer of 2 is an irreversible inhibitor, whereas the cis-isomer acts as a competitive inhibitor. In cells, the trans-isomer of compound 1 is completely inactive, whereas the cis-isomer inhibits histone H3-citrullination in a dose-dependent manner. Taken together, 1 serves as the foundation for developing photopharmaceuticals that can be activated at the desired tissue, using light, to treat diseases where PAD activity is dysregulated.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:Publisher
[do] DOI:10.1021/acschembio.8b00053

  7 / 81752 MEDLINE  
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[PMID]: 29512427
[Au] Autor:Koenig KA; Rao SM; Lowe MJ; Lin J; Sakaie KE; Stone L; Bermel RA; Trapp BD; Phillips MD
[Ad] Address:Imaging Institute, Cleveland Clinic, Cleveland, OH, USA.
[Ti] Title:The role of the thalamus and hippocampus in episodic memory performance in patients with multiple sclerosis.
[So] Source:Mult Scler;:1352458518760716, 2018 Mar 01.
[Is] ISSN:1477-0970
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Episodic memory loss is one of the most common cognitive symptoms in patients with multiple sclerosis (MS), but the pathophysiology of this symptom remains unclear. Both the hippocampus and thalamus have been implicated in episodic memory and show regional atrophy in patients with MS. OBJECTIVE: In this work, we used functional magnetic resonance imaging (fMRI) during a verbal episodic memory task, lesion load, and volumetric measures of the hippocampus and thalamus to assess the relative contributions to verbal and visual-spatial episodic memory. METHODS: Functional activation, lesion load, and volumetric measures from 32 patients with MS and 16 healthy controls were used in a predictive analysis of episodic memory function. RESULTS: After adjusting for disease duration, immediate recall performance on a visual-spatial episodic memory task was significantly predicted by hippocampal volume ( p < 0.003). Delayed recall on the same task was significantly predicted by volume of the left thalamus ( p < 0.003). For both memory measures, functional activation of the thalamus during encoding was more predictive than that of volume measures ( p < 0.002). CONCLUSION: Our results suggest that functional activation may be useful as a predictive measure of episodic memory loss in patients with MS.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:Publisher
[do] DOI:10.1177/1352458518760716

  8 / 81752 MEDLINE  
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[PMID]: 29478844
[Au] Autor:Peruzzotti-Jametti L; Bernstock JD; Vicario N; Costa ASH; Kwok CK; Leonardi T; Booty LM; Bicci I; Balzarotti B; Volpe G; Mallucci G; Manferrari G; Doneg M; Iraci N; Braga A; Hallenbeck JM; Murphy MP; Edenhofer F; Frezza C; Pluchino S
[Ad] Address:Department of Clinical Neurosciences and NIHR Biomedical Research Centre, University of Cambridge, Cambridge, UK. Electronic address: lp429@cam.ac.uk.
[Ti] Title:Macrophage-Derived Extracellular Succinate Licenses Neural Stem Cells to Suppress Chronic Neuroinflammation.
[So] Source:Cell Stem Cell;22(3):355-368.e13, 2018 Mar 01.
[Is] ISSN:1875-9777
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Neural stem cell (NSC) transplantation can influence immune responses and suppress inflammation in the CNS. Metabolites, such as succinate, modulate the phenotype and function of immune cells, but whether and how NSCs are also activated by such immunometabolites to control immunoreactivity and inflammatory responses is unclear. Here, we show that transplanted somatic and directly induced NSCs ameliorate chronic CNS inflammation by reducing succinate levels in the cerebrospinal fluid, thereby decreasing mononuclear phagocyte (MP) infiltration and secondary CNS damage. Inflammatory MPs release succinate, which activates succinate receptor 1 (SUCNR1)/GPR91 on NSCs, leading them to secrete prostaglandin E2 and scavenge extracellular succinate with consequential anti-inflammatory effects. Thus, our work reveals an unexpected role for the succinate-SUCNR1 axis in somatic and directly induced NSCs, which controls the response of stem cells to inflammatory metabolic signals released by type 1 MPs in the chronically inflamed brain.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review

  9 / 81752 MEDLINE  
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[PMID]: 29466830
[Au] Autor:Raheja R; Regev K; Healy BC; Mazzola MA; Beynon V; von Glehn F; Paul A; Diaz-Cruz C; Gholipour T; Glanz BI; Kivisakk P; Chitnis T; Weiner HL; Berry JD; Gandhi R
[Ad] Address:Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham & Women's Hospital, Harvard Medical School, Boston, USA.
[Ti] Title:Correlating serum microRNAs and clinical parameters in Amyotrophic lateral sclerosis.
[So] Source:Muscle Nerve;, 2018 Feb 21.
[Is] ISSN:1097-4598
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:INTRODUCTION: Amyotrophic lateral sclerosis (ALS) is a debilitating neurologic disorder with poor survival rates and no clear biomarkers for disease diagnosis and prognosis. METHODS: We compared serum miRNA expression from patients with ALS to healthy controls and patients with multiple sclerosis and Alzheimer's disease. We also correlated miRNA expression in cross-sectional and longitudinal cohorts of ALS patients with clinical parameters. RESULTS: We identified 7 microRNAs (miR-192-5p, miR-192-3p, miR-1, miR-133a-3p, miR-133b, miR-144-5p and miR-19a-3p) that were upregulated and 6 microRNAs (miR-320c, miR-320a, let-7d-3p, miR-425-5p, miR-320b and miR-139-5p) that were downregulated in ALS patients compared to healthy controls, Alzheimer's disease and multiple sclerosis patients. Changes in 4 miRNAs (miR-136-3p, miR-30b-5p, miR-331-3p, and miR-496) correlated positively and change in 1 microRNA (miR-2110) correlated negatively with changes in clinical parameters in longitudinal analysis. DISCUSSION: Our findings identified serum microRNAs that can serve as biomarkers for ALS diagnosis and progression. This article is protected by copyright. All rights reserved.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:Publisher
[do] DOI:10.1002/mus.26106

  10 / 81752 MEDLINE  
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[PMID]: 29392457
[Au] Autor:Landfeldt E; Castelo-Branco A; Svedbom A; Lfroth E; Kavaliunas A; Hillert J
[Ad] Address:Mapi Group, Stockholm, Sweden. erik.landfeldt@ki.se.
[Ti] Title:The long-term impact of early treatment of multiple sclerosis on the risk of disability pension.
[So] Source:J Neurol;265(3):701-707, 2018 Mar.
[Is] ISSN:1432-1459
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:OBJECTIVE: The objective of this retrospective, observational study was to estimate the long-term impact of early treatment of multiple sclerosis (MS) on the risk of disability pension. METHODS: Our cohort comprised patients with MS in Sweden, identified in a nationwide disease-specific register (the Swedish Multiple Sclerosis Registry), who started treatment with a disease-modifying drug (DMD) between January 1, 2002, and December 31, 2012. We analyzed the association between time from onset of MS to treatment initiation and full-time disability pension using survival analysis. RESULTS: Our sample comprised 2477 patients. Unadjusted Kaplan-Meier failure functions showed that patients who started treatment within six months after onset had a lower risk of disability pension across follow-up compared with patients initiating therapy after 12months. Outcomes from the univariate Cox proportional hazards model showed that time from onset to treatment initiation (in years) was significantly associated with disability pension (HR 1.03, p<0.001). Outcomes from the multivariable Cox proportional hazards model showed that patients who started treatment within 6months after onset had, on average, a 36% lower risk (HR 0.74, p=0.010) of full-time disability pension during follow-up compared with patients starting treatment after 18months when controlling for age, sex, marital status, university education, and prevalent comorbidities. CONCLUSIONS: We show that early treatment with DMDs of MS is associated with a significantly reduced risk of disability pension. Our findings highlight the potential long-term benefits of early treatment of MS and should be helpful to inform ongoing discussion on the optimum medical management of the disease.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process
[do] DOI:10.1007/s00415-018-8764-4


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