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Placebo-controlled phase 3 study of oral BG-12 for relapsing multiple sclerosis.
- R. Gold, L. Kappos, K. Dawson
- Medicine, PsychologyThe New England journal of medicine
- 19 September 2012
In patients with relapsing-remitting multiple sclerosis, both BG-12 regimens, as compared with placebo, significantly reduced the proportion of patients who had a relapse, the annualized relapse rate, the rate of disability progression, and the number of lesions on MRI.
Fumaric acid esters exert neuroprotective effects in neuroinflammation via activation of the Nrf2 antioxidant pathway.
The ability of dimethylfumarate to activate nuclear factor (erythroid-derived 2)-related factor 2 may offer a novel cytoprotective modality that further augments the natural antioxidant responses in multiple sclerosis tissue and is not yet targeted by other multiple sclerosis therapies.
Understanding pathogenesis and therapy of multiple sclerosis via animal models: 70 years of merits and culprits in experimental autoimmune encephalomyelitis research.
Critically discuss models of experimental autoimmune encephalomyelitis that reproduce specific features of the histopathology and neurobiology of multiple sclerosis and their shortcomings as tools to investigate emerging therapeutic approaches.
Distinct and nonredundant in vivo functions of IFNAR on myeloid cells limit autoimmunity in the central nervous system.
Siponimod versus placebo in secondary progressive multiple sclerosis (EXPAND): a double-blind, randomised, phase 3 study
Therapeutic efficacy of IL-17 neutralization in murine experimental autoimmune encephalomyelitis.
Spatial and temporal heterogeneity of mouse and human microglia at single-cell resolution
Insight is provided into the endogenous immune system of the central nervous system during development, homeostasis and disease, and may also provide new targets for the treatment of neurodegenerative and neuroinflammatory pathologies.
CNTF is a major protective factor in demyelinating CNS disease: A neurotrophic cytokine as modulator in neuroinflammation
A factor is identified that modulates, in an inflammatory environment, glial cell survival and is an outcome determinant of EAE, suggesting that endogenous CNTF may counterbalance this effect of TNF-α.
TNF receptor 1 genetic risk mirrors outcome of anti-TNF therapy in multiple sclerosis
This study demonstrates that clinical practice can be informed by comparing GWAS across common autoimmune diseases and by investigating the functional consequences of the disease-associated genetic variation.