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2,738 results for “multiple sclerosis”
Immune- and miRNA-response to Recombinant Interferon Beta in Healthy Volunteers and Patients With Relapsing Remitting Multiple Sclerosis
ClinicalTrials.gov study NCT02364986. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Delayed Diagnosis of Multiple Sclerosis, Treatment Initiation and Non-adherence in Upper Egypt
ClinicalTrials.gov study NCT05438693. IPD Sharing: NO. Countries: 1. Publications: 11.
Effect of High Intensity Interval Training in Patients With Multiple Sclerosis
ClinicalTrials.gov study NCT05954195. IPD Sharing: UNDECIDED. Countries: 1. Publications: 3.
Data from: Clinical correlation of multiple sclerosis immunopathological subtypes
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Effect of ocrelizumab on vaccine responses in patients with multiple sclerosis: The VELOCE study
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Data from: A randomized, placebo-controlled phase 2 trial of laquinimod in primary progressive multiple sclerosis
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Data from: Rituximab vs placebo induction prior to glatiramer acetate monotherapy in multiple sclerosis
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Association of gray matter atrophy patterns with clinical phenotype and progression in multiple sclerosis
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Data from: Plasma neurofilament light levels are associated with risk of disability in multiple sclerosis
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Data from: A survey of risk tolerance to multiple sclerosis therapies
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Data from: Is the association between health-related quality of life and fatigue mediated by depression in patients with multiple sclerosis? A Spanish cross sectional study
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Safety of ocrelizumab in patients with relapsing and primary progressive multiple sclerosis
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Supplemental tables for: A periventricular gradient of innate immune cell activation in Multiple Sclerosis
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Raw data related to: Sample Size for Oxidative Stress and Inflammation When Treating Multiple Sclerosis with Interferon-b1a and Coenzyme Q10
<p><strong>Abstract </strong></p> <p>Studying multiple sclerosis (MS) and its treatments requires the use of biomarkers for underlying pathological mechanisms. We aim to estimate the required sample size for detecting variations of biomarkers of inflammation and oxidative stress. This is a post-hoc analysis on 60 relapsing-remitting MS patients treated with Interferon-1a and Coenzyme Q10 for 3 months in an open-label crossover design over 6 months. At baseline and at the 3 and 6-month visits, we measured markers of scavenging activity, oxidative damage, and inflammation in the peripheral blood (180 measurements). Variations of laboratory measures (treatment eect) were estimated using mixed-eect linear regression models (including age, gender, disease duration, baseline expanded disability status scale (EDSS), and the duration of Interferon-1a treatment as covariates; creatinine was also included for uric acid analyses), and were used for sample size calculations. Hypothesizing a clinical trial aiming to detect a 70% eect in 3 months (power <strong>= </strong>80% alpha-error <strong>= </strong>5%), the sample size per treatment arm would be 1 for interleukin (IL)-3 and IL-5, 4 for IL-7 and IL-2R, 6 for IL-13, 14 for IL-6, 22 for IL-8, 23 for IL-4, 25 for activation-normal T cell expressed and secreted (RANTES), 26 for tumor necrosis factor (TNF)-, 27 for IL-1, and 29 for uric acid. Peripheral biomarkers of oxidative stress and inflammation could be used in proof-of-concept studies to quickly screen the mechanisms of action of MS treatments.</p> <p><strong>Progetto giovani ricercatori </strong>[GR-2016-02363725] dal titolo: "Immune Tolerance, Metabolism and Multiple Sclerosis: Novel Molecular Tools to Monitor Disease Pathogenesis and Progression"</p>
Raw data related to: Coenzyme Q10 supplementation reduces peripheral oxidative stress and inflammation in interferon-β1a-treated multiple sclerosis
<p><strong>Abstract</strong></p> <p>Background: Oxidative stress is a driver of multiple sclerosis (MS) pathology. We evaluated the effect of coenzyme Q10 (CoQ10) on laboratory markers of oxidative stress and inflammation, and on MS clinical severity.</p> <p>Methods: We included 60 relapsing–remitting patients with MS treated with interferon beta1a 44<strong>μ</strong>g (IFN-<strong>β</strong>1a) with CoQ10 for 3 months, and with IFN-<strong>β</strong>1a 44<strong>μ</strong>g alone for 3 more months (in an open-label crossover design). At baseline and at the 3 and 6-month visits, we measured markers of scavenging activity, oxidative damage and inflammation in the peripheral blood, and collected data on disease severity.</p> <p>Results: After 3 months, CoQ10 supplementation was associated with improved scavenging activity (as mediated by uric acid), reduced intracellular reactive oxygen species production, reduced oxidative DNA damage, and a shift towards a more anti-inflammatory milieu in the peripheral blood [with higher interleukin (IL)-4 and IL-13, and lower eotaxin, granulocyte-macrophage colonystimulating factor (GM-CSF), hepatocyte growth factor (HGF), interferon (IFN)-<strong>γ</strong>, IL-1<strong>α</strong>, IL-2R, IL-9, IL-17F, macrophage inflammatory proteins (MIP)-1<strong>α</strong>, regulated on activation-normal T cell expressed and secreted (RANTES), tumor necrosis factor (TNF)-<strong>α</strong>, and vascular endothelial growth factor (VEGF). Also, CoQ10 supplementation was associated with lower Expanded Disability Status Scale, fatigue severity scale, Beck’s depression inventory, and the visual analogue scale for pain.</p> <p>Conclusions: CoQ10 supplementation improved scavenging activity, reduced oxidative damage, and induced a shift towards a more anti-inflammatory milieu, in the peripheral blood of relapsing–remitting MS patients treated with 44<strong>μ</strong>g IFN-<strong>β</strong>1a 44<strong>μ</strong>g. A possible clinical effect was noted but deserves to be confirmed over longer follow ups.</p> <p><strong>Progetto giovani ricercatori </strong>[GR-2016-02363725] dal titolo: "Immune Tolerance, Metabolism and Multiple Sclerosis: Novel Molecular Tools to Monitor Disease Pathogenesis and Progression"</p>
Raw data relative to: "Distinct Expression of Inflammatory Features in T Helper 17 Cells from Multiple Sclerosis Patients"
<p><strong>Introduction</strong></p> <p> Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS). T helper (Th) 17 lymphocytes play a role in the pathogenesis of MS. Indeed, Th17 cells are abundant in the cerebrospinal fluid and peripheral blood of MS patients and promote pathogenesis in the mouse model of MS. To gain insight into the function of Th17 cells in MS, we tested whether Th17 cells polarized from naïve CD4 T cells of healthy donors and MS patients display different features</p> <p><strong>Methods</strong></p> <p>We analysed several parameters that typify the Th17 profile during the differentiation process of naïve CD4 T cells obtained from relapsing-remitting (RR)-MS patients and healthy donors (HD), such as expression of surface receptors by flow cytometry.</p> <p><strong>Results</strong></p> <p>The analysis revealed that expression of IL-1R1 is significantly increased in Th17 cells derived from MS patients compared to healthy donor-derived cells. Interestingly, IL-1R1 expression is also increased in Th17 cells circulating in the blood of MS patients compared to healthy donors. Since IL-1R1 play a crucial role in the activation of immune cells, our data indicate that high expression of these molecules in Th17 cells from MS patients could be related to their high inflammatory status.</p>
Data from: Head-to-head drug comparisons in multiple sclerosis: urgent action needed
Disease-modifying drugs are changing the natural history of multiple sclerosis (MS). However, currently available clinical trial data are insufficient to develop accurate personalised treatment algorithms to assign the best possible treatment to each person with MS according to disease features, treatment history and comorbidities. Such accurate algorithms would require the presence of numerous head-to-head trials of long duration, which is virtually impossible, given the economic costs, required time and difficulties with attrition. Thus, efforts are being made to compare relative treatment efficacy through observational designs, using large multi-centre prospective cohorts or 'big MS data', and network meta-analyses. Although such studies can yield useful information, they are liable to biases and their results should be confirmed in other study populations, including smaller, single-centre cohorts, where some of these biases can be minimised. In this View paper we analyse the potential benefits and biases of all these strategies alternative to head-to-head trials in MS. Finally, we propose the combination of all these types of studies to obtain reliable head-to-head drug comparisons in the absence of randomised designs.
Data from: Quantitative benefit-risk assessment of methylprednisolone in multiple sclerosis relapses
Background: High-dose short-term methylprednisolone is the recommended treatment in the management of multiple sclerosis relapses, although it has been suggested that lower doses may be equally effective. Also, glucocorticoids are associated with multiple and often dose-dependent adverse effects. This quantitative benefit-risk assessment compares high- and low-dose methylprednisolone (at least 2000 mg and less than 1000 mg, respectively, during at most 31 days) and a no treatment alternative, with the aim of determining which regimen, if any, is preferable in multiple sclerosis relapses. Methods: An overall framework of probabilistic decision analysis was applied, combining data from different sources. Effectiveness as well as risk of non-serious adverse effects were estimated from published clinical trials. However, as these trials recorded very few serious adverse effects, risk intervals for the latter were derived from individual case reports together with a range of plausible distributions. Probabilistic modelling driven by logically implied or clinically well motivated qualitative relations was used to derive utility distributions. Results: Low-dose methylprednisolone was not a supported option in this assessment; there was, however, only limited data available for this treatment alternative. High-dose methylprednisolone and the no treatment alternative interchanged as most preferred, contingent on the risk distributions applied for serious adverse effects, the assumed level of risk aversiveness in the patient population, and the relapse severity. Conclusions: The data presently available do not support a change of current treatment recommendations. There are strong incentives for further clinical research to reduce the uncertainty surrounding the effectiveness and the risks associated with methylprednisolone in multiple sclerosis relapses; this would enable better informed and more precise treatment recommendations in the future.
Data from: Effect of dalfampridine on information processing speed impairment in multiple sclerosis
Objective: To test a possible benefit of dalfampridine on information processing speed (IPS), a key function for cognitive impairment (CogIm) in multiple sclerosis (MS). Methods: In this randomized, double-blind, placebo-controlled trial, we included patients with a score on the Symbol Digit Modalities Test (SDMT) under the 10th percentile of the reference value. Patients were randomized in a 2:1 ratio to receive dalfampridine 10 mg or placebo twice daily for 12 weeks. They underwent a comprehensive neuropsychological evaluation at screening (T0), at the end of treatment (T1), and after a 4-week follow-up (T2). The primary endpoint was improvement in SDMT. Results: Out of 208 patients screened, 120 were randomized to receive either dalfampridine (n = 80) or placebo (n = 40). At T1, the dalfampridine group presented an increase of SDMT scores vs placebo group (mean change 9.9 [95% confidence interval (CI) 8.5–11.4] vs 5.2 [95% CI 2.8–7.6], p = 0.0018; d = 0.60 for raw score; and 0.8 [95% CI 0.6–1] vs 0.3 [95% CI 0.0–0.5], p = 0.0013; d = 0.61 for z scores; by linear mixed model with robust standard error). The improvement was not sustained at T2. A beneficial effect of dalfampridine was observed in the Paced Auditory Serial Addition Test and in cognitive fatigue. Conclusion: Dalfampridine could be considered as an effective treatment option for IPS impairment in MS. Trial registration: 2013-002558-64 EU Clinical Trials Register. Classification of evidence: This study provides Class I evidence that for patients with MS with low scores on the SDMT, dalfampridine improves IPS.
Data from: Onset of clinical and MRI efficacy of ocrelizumab in relapsing multiple sclerosis
Objective: To assess the onset of ocrelizumab efficacy on brain magnetic resonance imaging (MRI) measures of disease activity in the Phase II study in relapsing-remitting multiple sclerosis (RRMS), and relapse rate in the pooled Phase III studies in relapsing multiple sclerosis (RMS). Methods: Brain MRI activity was determined in the Phase II trial at monthly intervals in patients with RRMS receiving placebo, ocrelizumab (600 mg), or intramuscular interferon (IFN) β-1a (30 μg). Annualized relapse rate (ARR; over various epochs) and time to first relapse were analyzed in the pooled population of the Phase III OPERA I and OPERA II trials in patients with RMS receiving ocrelizumab (600 mg) or subcutaneous IFN β-1a (44 μg). Results: In patients with RRMS, ocrelizumab reduced the number of new T1 gadolinium-enhancing lesions by Week 4 vs placebo (p=0.042) and by Week 8 vs intramuscular IFN β-1a (p<0.001). Ocrelizumab also reduced the number of new or enlarging T2 lesions appearing between Weeks 4 and 8 vs both placebo and IFN β-1a (both p<0.001). In patients with RMS, ocrelizumab significantly reduced ARR (p=0.005), and the probability of time to first protocol-defined relapse (p=0.014) vs subcutaneous IFN β-1a within the first 8 weeks. Conclusion: Epoch analysis of MRI-measured lesion activity in the Phase II study and relapse rate in the Phase III studies consistently revealed a rapid suppression of acute MRI and clinical disease activity following treatment initiation with ocrelizumab in patients with RRMS and RMS, respectively. Classification of evidence: This study provides Class II evidence that for patients with RRMS and RMS, ocrelizumab suppressed MRI activity within 4 weeks and clinical disease activity within 8 weeks.
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.