Effect of Glatiramer Acetate on Peripheral Blood Brain-Derived Neurotrophic Factor and Phosphorylated TrkB Levels in Relapsing- Remitting Multiple Sclerosis

Author(s): Vitalie Vacaras, Zsigmond Z. Major, Dafin F. Muresanu, Tibor L. Krausz, Ioan Marginean, Dana A. Buzoianu.

Journal Name: CNS & Neurological Disorders - Drug Targets
(Formerly Current Drug Targets - CNS & Neurological Disorders)

Volume 13 , Issue 4 , 2014

Become EABM
Become Reviewer

Abstract:

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.

Keywords: Brain-derived neurotrophic factor, glatiramer acetate, multiple sclerosis, receptor tyrosine kinase B.

Rights & PermissionsPrintExport Cite as

Article Details

VOLUME: 13
ISSUE: 4
Year: 2014
Page: [647 - 651]
Pages: 5
DOI: 10.2174/1871527313666140618110049
Price: $58

Article Metrics

PDF: 24