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dc.contributor.advisorChumley, Michael J.
dc.contributor.authorMitchel, Jeffrey Stewart,Jren_US
dc.date.accessioned2014-07-22T18:48:39Z
dc.date.available2014-07-22T18:48:39Z
dc.date.created2012en_US
dc.date.issued2012en_US
dc.identifierUMI thesisen_US
dc.identifieretd-05042012-131204en_US
dc.identifierumi-10306en_US
dc.identifiercat-001821246en_US
dc.identifier.urihttps://repository.tcu.edu:443/handle/116099117/4416
dc.description.abstractHeat shock proteins (Hsps) serve as the cell's natural mechanism for circumventing protein misfolding and aggregation often involved in cellular stress. These stressors can lead to neurodegenerative pathologies like Alzheimer's disease (AD). Research suggests that aged animals lose the ability to upregulate Hsps in response to an acute stress, and this disregulation may contribute to the onset of AD. We hypothesize that aged animals will show elevated Hsp levels due to the increase in cellular stress associated with aging. We further hypothesize that this increased level of Hsps will inhibit the aged animal from further expressing Hsps in the event of an acute stress. We compared basal and inducible brain hippocampus levels of four Hsps previously shown to stabilize two proteins commonly associated with AD, amyloid beta and tau. Our results support our hypothesis that Hsp expression changes with age and may be a contributing factor in AD.en_US
dc.format.mediumFormat: Onlineen_US
dc.publisher[Fort Worth, Tex.] : Texas Christian University,en_US
dc.relation.ispartofTCU Master Thesisen_US
dc.relation.requiresMode of access: World Wide Web.en_US
dc.relation.requiresSystem requirements: Adobe Acrobat reader.en_US
dc.titleAge-related changes in heat shock protein expression in the mouse hippocampusen_US
dc.typeTexten_US
etd.degree.departmentDepartment of Biology
etd.degree.levelMaster
local.collegeCollege of Science and Engineering
local.departmentBiology
local.academicunitDepartment of Biology
dc.type.genreThesis
local.subjectareaBiology
etd.degree.nameMaster of Science


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