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A randomized, placebo-controlled trial of natalizumab for relapsing multiple sclerosis.
TLDR
Natalizumab reduced the risk of the sustained progression of disability and the rate of clinical relapse in patients with relapsing multiple sclerosis and hold promise as an effective treatment for relapsed multiple sclerosis.
Placebo-controlled phase 3 study of oral BG-12 for relapsing multiple sclerosis.
TLDR
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.
Ocrelizumab versus Placebo in Primary Progressive Multiple Sclerosis
TLDR
Among patients with primary progressive multiple sclerosis, ocrelizumab was associated with lower rates of clinical and MRI progression than placebo; there was no clinically significant difference between groups in the rates of serious adverse events and serious infections.
Ocrelizumab versus Interferon Beta‐1a in Relapsing Multiple Sclerosis
TLDR
Among patients with relapsing multiple sclerosis, ocrelizumab was associated with lower rates of disease activity and progression than interferon beta‐1a over a period of 96 weeks.
A placebo-controlled trial of oral cladribine for relapsing multiple sclerosis.
TLDR
Treatment with cladribine tablets significantly reduced relapse rates, the risk of disability progression, and MRI measures of disease activity at 96 weeks, and the benefits need to be weighed against the risks.
A ChIP-seq defined genome-wide map of vitamin D receptor binding: associations with disease and evolution.
TLDR
ChIP-seq determination of transcription factor binding, in combination with GWA data, provides a powerful approach to further understanding the molecular bases of complex diseases.
The peripheral benzodiazepine binding site in the brain in multiple sclerosis: quantitative in vivo imaging of microglia as a measure of disease activity.
This study identifies by microautoradiography activated microglia/macrophages as the main cell type expressing the peripheral benzodiazepine binding site (PBBS) at sites of active CNS pathology.
Direct suppression of CNS autoimmune inflammation via the cannabinoid receptor CB1 on neurons and CB2 on autoreactive T cells
TLDR
The results demonstrate that the cannabinoid system within the CNS plays a critical role in regulating autoimmune inflammation, with the CNS directly suppressing T-cell effector function via the CB2 receptor.
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