Axonopathy in peripheral myelin protein 22 insufficiency

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dc.contributor.advisor Bishop, Derron L. Zamani, Atiq 2011-06-09T15:25:50Z 2011-06-09T15:25:50Z 2010-07-24 en_US 2010-07-24
dc.description.abstract The role that various myelin membrane proteins play during development and disease processes is not well understood. To better understand their role in vivo we have crossed transgenic mice possessing a single truncated pmp22 gene with mice expressing yellow fluorescent protein in the cytoplasm of their neurons. The resulting double transgenic mice were examined by a combination of confocal microscopy, transmission electron microscopy, and immunohistochemistry to determine if pmp22 insufficiency alters the structural integrity of myelin, glial cells, axons, or the subcellular milieu of these various components. Axons from mice with pmp22 insufficiency developed sprouts and debris localized to nodes with no signs of degeneration of a Wallerian type. Ultrastructurally, the nodes accumulated tubovesicular structures as well as disrupted cytoskeleton that did not appear to alter axon transport. Together, these results suggest that pmp22 insufficiency leads to a non-lethal axonopathy that is restricted to nodes.
dc.description.sponsorship Department of Physiology and Health Science
dc.subject.lcsh Axons.
dc.subject.lcsh Myelin proteins.
dc.subject.lcsh Demyelination -- Genetic aspects.
dc.subject.lcsh Mice -- Nervous system.
dc.title Axonopathy in peripheral myelin protein 22 insufficiency en_US
dc.title.alternative Title on signature sheet: Axonopathy in peripheral myelin protein22 (pmp22) insufficiency Thesis (M.S.)

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  • Master's Theses [5318]
    Master's theses submitted to the Graduate School by Ball State University master's degree candidates in partial fulfillment of degree requirements.

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