alexa Gas6/Axl Requirement For Taming Inflammation And Enhancing Remyelination
ISSN: 2329-6895

Journal of Neurological Disorders
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2nd International Conference on Neuroimmunology & Therapeutics
December 01-02, 2016 Atlanta, USA

Bridget Shafit-Zagardo
Albert Einstein College of Medicine, USA
Posters & Accepted Abstracts: J Neurol Disord
DOI: 10.4172/2329-6895.C1.015
Abstract
MS is a disease of unknown etiology in which the body’s immune cells target myelin, the protective and insulating coating of nerves in the CNS. The CNS damage resulting from MS causes wide-ranging symptoms in the estimated 2.3 million people affected by the disease worldwide. Several animal models of demyelinating diseases aid in the study of MS, including myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis (MOG-induced EAE) and cuprizone induced demyelination/remyelination. Gas6 is the sole ligand for the Axl receptor, a member of the Tyro3/Axl/ Mertk family of receptor tyrosine kinases shown to have anti-inflammatory and promyelinating effects. Previous research demonstrates that Gas6-/- and/or Axl-/- single knockout mice undergo more severe demyelination and more inflammation than WT mice in response to EAE. Additionally, delivery of Gas6 to the CNS dampens the immune response and improves the clinical outcome of this disease. Furthermore, cuprizone fed Axl-/- and Gas6-/- mice exhibit a lag in debris clearance, contributing to their delay in recovery. Current studies are examining the disease course and remyelination process of EAE and the cuprizone model, respectively, in Axl-/-Gas6-/- double knockout mice (DKO). The DKO mice display an atypical EAE disease course demonstrating that Gas6-Axl signaling may play a crucial role in the disease. Furthermore, DKO mice show little to no remyelination in the cuprizone model, as well as significantly fewer oligodendrocytes in the corpus callosum at 5 weeks and 6 weeks, and axonal damage at 6 weeks cuprizone+3-weeks cuprizone withdrawal compared to WT mice.
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