Glatiramer acetate (GA) is one of the most widely used disease-modifying drugs for the treatment of relapsingremitting
multiple sclerosis; is assumed to have inductor effects on neurotrophic factor expression. One of these
neurotrophic factor systems is the brain-derived neurotrophic factor (BDNF)/receptor tyrosine kinase B (TrkB) pathway.
Peripheral blood is thought to contain soluble BDNF, and some blood cells express TrkB. We attempted to determine
whether GA treatment leads to changes in plasma BDNF levels and TrkB activation. Such a phenomenon are relapsingremitting
multiple sclerosis patients is significantly reduced; GA treatment is not influencing peripheral BDNF levels,
after one year of sustained therapy, not from the point of view of total free BDNF nor the phosphorylated TrkB.