Latest News

Gut microbiome and MS pathogenesis

 

REPORT FROM THE ACTRIMS-ECTRIMS – BOSTON, MA, SEPTEMBER 10-13, 2014 – Several lines of evidence indicate that the gut microbiome plays a role in the pathogenesis of MS. It has been suggested that environmental risk factors, such as diet, vitamin D insufficiency, obesity and smoking, may contribute to alterations in the GI flora that may predispose to autoimmune dysregulation (Joscelyn & Kasper. Mult Scler 2014; epublished July 28, 2014).

Gut flora, such as Bacteroides fragilis, produce short-chain fatty acids which have been shown in animal models to have anti-inflammatory effects on peripheral immune cells and which are involved in the proliferation of regulatory T cells (Tregs) (Smith et al. Science 2013;341:569-573; Maslowski et al. Nature 2009;461:1282-1286; Furusawa et al. Nature 2013;504:446-450). Read More

NEDA: an emerging concept in MS

 

REPORT FROM THE ACTRIMS-ECTRIMS – BOSTON, MA, SEPTEMBER 10-13, 2014 – The assessment of treatment response has evolved over the past two decades of DMT use, with early trials focusing on relapse rates and disability progression. Indeed, the pivotal trial of glatiramer acetate did not evaluate the effect of treatment on MRI (Johnson et al. Neurology 1995;45:1268-1276).

Since that time, individual clinical (relapses, EDSS) and radiological measures have become the gold standard for evaluating treatment effects, although a number of authors have reported that combining metrics may have prognostic value (Sormani et al. Mult Scler 2013;19:605-612). Read More

Clinical trial recruitment: what do patients think?

 

REPORT FROM THE ACTRIMS-ECTRIMS – BOSTON, MA, SEPTEMBER 10-13, 2014 – The proliferation of new treatments in development for MS has made it increasingly challenging to recruit a sufficient number of eligible study subjects, most notably for studies involving pediatric or untreated patients. Read More

Dietary salt may worsen MS

 

REPORT FROM THE ACTRIMS-ECTRIMS – BOSTON, MA, SEPTEMBER 10-13, 2014 – Recent studies have indicated that increased sodium chloride concentrations can induce pathogenic CD4+ Th17 cells in humans (Kleinewietfeld et al. Nature 2013;496:518-522; free full text at www.ncbi.nlm.nih.gov/pmc/articles/PMC3746493/pdf/nihms500370.pdf). This effect is specific to Th17, with little or no effect on Th1 or Th2 differentiation or proliferation. Moreover, salt-induced Th17 cells demonstrate increased production of pro-inflammatory cytokines, such as TNF-alpha and IL-2. Read More