Abstract Details

Title Copaxone Treatment Inhibits Axon Degeneration, Restores Axon Conduction and Improves Motor Activity of Experimental Autoimmune Encephalomyelitis Mice

Topic MS and Related Diseases

Presentation(s) P05 - (-)

Poster/Presentation
Number 161

Objective

Background BACKGROUND: Glatiramer acetate (GA Copaxone Copolymer 1) is an approved drug for the treatment of MS. It is an anti-inflammatory and immunomodulatory agent that can also be directly neuroprotective in the EAE model. The underlying multifactorial anti-inflammatory-neuroprotective effect of Copaxone is in the induction of reactive T-cells that release immunomodulatory cytokines and neurotrophic factors at the injury site. These Copaxone treatment-induced cytokines and growth factors may have a direct effect on axon function.

Design/Methods DESIGN/METHODS: 8-week-old PLP_EGFP C57BL/6 mice were treated with Copaxone at a concentration of 2 mg/ mouse/day for 8 days. Treatment groups received daily Copaxone injections starting post-day 14 after first MOG immunization. Mean clinical scores and rotorod motor tests of various EAE groups were assessed two to three times per week. Electrophysiology conduction of corpus callosum axons and immunohistochemistry of brain and spinal cord were performed 38-42 days post-disease induction.

Results RESULTS: Mean clinical disease scores of Copaxone-treated EAE mice compared to vehicle-treated mice, were significantly reduced throughout disease. Copaxone treatment significantly improved callosal conduction of myelinated and non-myelinated axons in EAE mice to normal levels in contrast to vehicle-treated EAE mice. Increased numbers of myelinated fibers with intact nodes were observed in the corpus callosum of Copaxone-treated EAE group by immunohistochemical analysis. In addition, Copaxone treatment significantly increased the amount of time the mice spent on the rotorod compared to vehicle treated mice. This was supported by an increase in myelinated axons and fewer b-APP positive axons in the spinal cords of treated mice.

Conclusions CONCLUSIONS: Our results show that Copaxone significantly improves axon function due to its positive effects on myelinated and non-myelinated axons in the EAE model.

Authors/Disclosures
Spencer Moore PRESENTER	No disclosure on file
	No disclosure on file
	No disclosure on file
Peter B. Kang, MD, FAAN (University of Minnesota Medical School)	Dr. Kang has received personal compensation in the range of $5,000-$9,999 for serving as a Consultant for Neurogene. Dr. Kang has received personal compensation in the range of $500-$4,999 for serving as a Consultant for Lupin. Dr. Kang has received personal compensation in the range of $500-$4,999 for serving as a Consultant for ITF Therapeutics (Italfarmaco). An immediate family member of Dr. Kang has received personal compensation in the range of $0-$499 for serving as a Consultant for Life Sciences Consultants. Dr. Kang has received personal compensation in the range of $500-$4,999 for serving on a Scientific Advisory or Data Safety Monitoring board for MLAB Biosciences. Dr. Kang has received personal compensation in the range of $10,000-$49,999 for serving as an Editor, Associate Editor, or Editorial Advisory Board Member for Wiley. Dr. Kang has received personal compensation in the range of $10,000-$49,999 for serving as an Editor, Associate Editor, or Editorial Advisory Board Member for ��ɫ��. The institution of Dr. Kang has received research support from Xtraordinary Joy Foundation. The institution of an immediate family member of Dr. Kang has received research support from Sarepta Therapeutics. The institution of Dr. Kang has received research support from Centers for Disease Control and Prevention (CDC). The institution of Dr. Kang has received research support from National Institutes of Health (NIH). The institution of Dr. Kang has received research support from Food and Drug Administration. The institution of Dr. Kang has received research support from National Initiative for Cockayne Syndrome. The institution of Dr. Kang has received research support from Greg Marzolf Jr Foundation. The institution of Dr. Kang has received research support from Sarepta Therapeutics. The institution of Dr. Kang has received research support from Duchenne UK - PPMD. The institution of an immediate family member of Dr. Kang has received research support from Regenerative Medicine MN. The institution of an immediate family member of Dr. Kang has received research support from Greg Marzolf Jr Foundation. The institution of an immediate family member of Dr. Kang has received research support from NIH. The institution of an immediate family member of Dr. Kang has received research support from Viljem Julijan Association for Children with Rare Disease. The institution of Dr. Kang has received research support from Minnesota Partnership. Dr. Kang has received intellectual property interests from a discovery or technology relating to health care. An immediate family member of Dr. Kang has received intellectual property interests from a discovery or technology relating to health care. Dr. Kang has received publishing royalties from a publication relating to health care. Dr. Kang has a non-compensated relationship as a Medical Advisory Board with Speak Foundation that is relevant to AAN interests or activities. Dr. Kang has a non-compensated relationship as a President (Including President-Elect and Past President) with Child Neurology Society that is relevant to AAN interests or activities. Dr. Kang has a non-compensated relationship as a Board Member with Child Neurology Foundation that is relevant to AAN interests or activities.
	No disclosure on file
	No disclosure on file
Seema K. Tiwari-Woodruff, PhD (School of Medicine at UCR)	No disclosure on file

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