Abstract
Multiple sclerosis (MS) is a neurodegenerative disorder caused by a prolonged immune- mediated inflammatory response that targets myelin. Nearly all of the drugs approved for the treatment of MS are general immunosuppressants or only function in symptom management. The oral medication fingolimod, however, is reported to have direct therapeutic effects on cells of the central nervous system in addition to immunomodulatory functions. Fingolimod is known to interact with sphingosine-1-phosphate (S1P) receptors, and the most widely- accepted theory for its mechanism of action is functional antagonism of the receptor. This review examines significant neuromodulatory effects achieved by functional antagonism of the receptors S1P1 and S1P3 on astrocytes and speculates on the potential role of S1P receptors in the pathogenesis of MS.
Recommended Citation
Crawford, Madelyn Elizabeth
(2014)
"FTY720 (Fingolimod) Provides Insight into the Molecular Mechanisms of Multiple Sclerosis,"
Pursuit - The Journal of Undergraduate Research at The University of Tennessee: Vol. 5
:
Iss.
1
, Article 7.
Available at:
https://trace.tennessee.edu/pursuit/vol5/iss1/7
Included in
Biological Phenomena, Cell Phenomena, and Immunity Commons, Biology Commons, Cell Biology Commons, Immune System Diseases Commons, Immunopathology Commons, Medical Cell Biology Commons, Medical Immunology Commons, Medical Microbiology Commons, Medical Molecular Biology Commons, Medical Neurobiology Commons, Medical Pharmacology Commons, Molecular and Cellular Neuroscience Commons, Musculoskeletal, Neural, and Ocular Physiology Commons, Nervous System Diseases Commons, Neurosciences Commons, Other Immunology and Infectious Disease Commons, Other Microbiology Commons, Other Neuroscience and Neurobiology Commons