Testosterone Mediated Neuroprotection from FasL Induced Apoptosis within Purkinje Cells
| dc.contributor.advisor | Bryant, Damani | |
| dc.contributor.author | Mike, Luke | |
| dc.date.accessioned | 2015-01-09T21:16:49Z | |
| dc.date.available | 2015-01-09T21:16:49Z | |
| dc.date.issued | 2014-04 | |
| dc.description | Color poster with text, charts, graphs, and images. | en |
| dc.description.abstract | Over the years, the cerebellum has been noted to play a prominent role in the incidence of neurodevelopmental disorders. These disease states have a higher incidence in males than females. From birth, through the first three postnatal weeks, PCs (Purkinje Cells) will form synaptic junctions as well as go through a period of programmed cell death. This also happens to be around the time when Granule Cell Progenitors (GCP) will migrate through the PC layer. As this migration occurs, a number of signals will be sent back and forth between GCP and PCs which is critically responsible for proper development. One potential signal is the Fas ligand (FasL), an apoptotic inducer of programmed cell death. FasL is noted to play a critical role in neurodevelopment. Testosterone has the ability to neuroprotect against apoptotic death. The purpose of this study was to determine whether PCs are indeed susceptible to FasL induced apoptotic death and to see if male PCs are more resistance to this death due to testosterone. | en |
| dc.description.sponsorship | University of Wisconsin--Eau Claire Office of Research and Sponsored Programs. | en |
| dc.identifier.uri | http://digital.library.wisc.edu/1793/70185 | |
| dc.language.iso | en_US | en |
| dc.relation.ispartofseries | USGZE AS589 | en |
| dc.subject | Testosterone--Role of | en |
| dc.subject | Fas Ligand (FasL) | en |
| dc.subject | Purkinje Cells (PCs) | en |
| dc.subject | Neurodevelopmental disorders | en |
| dc.subject | Posters | en |
| dc.title | Testosterone Mediated Neuroprotection from FasL Induced Apoptosis within Purkinje Cells | en |
| dc.type | Presentation | en |
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