Phenotypic Plasticity Research Experience for Community College Students

Document Type


Publication Date

Summer 2019


Multiple Sclerosis (MS) is an autoimmune inflammatory disease of the central nervous system. MS is characterized by episodes of demyelination followed by partial remyelination. Cuprizone is a toxin that causes demyelination in specific regions of the C57BL/6 mouse brain, which remyelinate upon termination of cuprizone. Upper respiratory infections are known to exacerbate MS symptoms We hypothesize that infection may impede remyelination, possibly due to a direct effect on oligodendrocyte maturation. If this is the case, we may find a reduced amount of mature oligodendrocytes and large amounts of oligodendrocyte precursor cells (OPCs) in areas of heavy demyelination in flu mice compared to controls.The aim of this study is to observe the impact of peripheral infection on remyelination in the corpus callosum, a known area of heavy demyelination in the cuprizone model.


Copyright is owned by the creators of this work.


This project was completed with the cooperation of Dr. Steelman's Laboratory,, Department of Animal Sciences, University of Illinois at Urbana-Champaign.

Financial support was provided by the NationalScience Foundation under grant #NSF REU 1559908/1559929, as part of the Phenotypic Plasticity Research Experience for Community College Students, through the University of Illinois at Urbana-Champaign Institute for Genomic Biology and Parkland College. Financial support also provided by the National Multiple Sclerosis Society RF-1807-32053 as well as the ACES FIRE grant ILLU-971-353



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