Multiple Sclerosis Discovery Forum

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New Data Show Longer Tysabri Dosing Interval in MS Is Feasible
SIRT1 Deficiency in Microglia Contributes to Cognitive Decline in Aging and Neurodegeneration via Epigenetic Regulation of IL-1β.
Consensus Recommendations for the Diagnosis and Treatment of Multiple Sclerosis The Middle East North Africa Committee for Treatment and Research in Multiple Sclerosis (MENACTRIMS).
Mirna-Mediated Macrophage Polarization and its Potential Role in the Regulation of Inflammatory Response.
Tolerance induced by apoptotic antigen-coupled leukocytes is induced by PD-L1+ and IL-10-producing splenic macrophages and maintained by T regulatory cells.
Demyelination and other neurological adverse events after anti-TNF therapy.
[Retinal vasculitis as manifestation of multiple sclerosis.]
A validated regulatory network for Th17 cell specification.
How type I interferons shape myeloid cell function in CNS autoimmunity.
IL-17: A new actor in IFN-driven systemic autoimmune diseases.
We are about to cure multiple sclerosis in the next 10 years, even though we do not know its cause: Yes.
Vitamin d and multiple sclerosis.
Distinct lesion morphology at 7-T MRI differentiates neuromyelitis optica from multiple sclerosis.
Drug therapy for multiple sclerosis.
IL-17 induces MIP-1α expression in primary mouse astrocytes via TRPC channel.
Glial Cell Development and Function in Zebrafish.
Medical marijuana in neurology.
IFNβ secreted by microglia mediates clearance of myelin debris in CNS autoimmunity.
Cognitive reserve in multiple sclerosis: Protective effects of education.
Does jcv antibody positivity encourage cessation of natalizumab therapy in multiple sclerosis?
Recurrent Varicella following Steroids and Fingolimod in a Multiple Sclerosis Patient.
Health care-resource utilization before and after natalizumab initiation in multiple sclerosis patients in the US.
Multimodal noninvasive and invasive imaging of extracranial venous abnormalities indicative of CCSVI: results of the PREMiSe pilot study.
Characterization of the interaction between astrocytes and encephalitogenic lymphocytes during the development of experimental autoimmune encephalitomyelitis (EAE) in mice.
Suppression of the lipid peroxidation process in the CNS reduces neurological expression of experimentally induced autoimmune encephalomyelitis.

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