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dc.contributor.advisorZabel, Mark
dc.contributor.advisorTjalkens, Ronald B.
dc.contributor.authorRocha, Savannah M.
dc.contributor.committeememberBouma, Jerry
dc.contributor.committeememberKading, Rebekah
dc.contributor.committeememberMoreno, Julie
dc.date.accessioned2022-08-29T10:17:25Z
dc.date.available2023-08-22T10:17:25Z
dc.date.issued2022
dc.description2022 Summer.
dc.descriptionIncludes bibliographical references.
dc.description.abstractParkinson's Disease (PD) is the world's foremost movement disorder with pathological features including loss of dopaminergic neurons (DAn) within the substantia nigra pars compacta (SNpc), chronic activation of glial cells, and the misfolding and aggregation of a-synuclein (a-syn). Compounding evidence gathered over the past two centuries suggests environmental exposures, genetics, and aging can induce complicated cell-to-cell interactions that evoke and facilitate chronic inflammatory states; but the role that individual glial cells, in particular microglia, have in the progression of disease remains unknown. Difficulties in recapitulating the three pathological hallmarks of PD underscore the need for better animal models. To address this gap in functional investigation, the studies herein provide, for the first time, an optimized environmental exposure model with the pesticide rotenone (2.5mg/kg/day) in murine, which has proven effective at mirroring DAn degeneration, gliosis and misfolded a-syn accumulation. The pathology observed was region-, time- and dose-dependent, emphasizing the importance of environmental exposure and associated PD diagnosis. The successful optimization of this exposure model has allowed for its implementation in transgenic mice, which was previously unfeasible. To determine microglial specific innate inflammatory reactions in the progression of PD, we targeted the inflammatory transcriptional regulator NF-kB by use of transgenic CX3CR1-Cre
dc.format.mediumborn digital
dc.format.mediumdoctoral dissertations
dc.identifierRocha_colostate_0053A_17387.pdf
dc.identifier.urihttps://hdl.handle.net/10217/235733
dc.languageEnglish
dc.publisherColorado State University. Libraries
dc.relation.ispartof2020- CSU Theses and Dissertations
dc.rightsCopyright of the original work is retained by the author.
dc.rights.accessEmbargo Expires: 08/22/2023
dc.subjectglia
dc.subjectneuroscience
dc.subjectprotein misfolding
dc.subjectmicroglia
dc.subjectastrocytes
dc.subjectParkinson's disease
dc.titleMicroglial innate and adaptive immune function modulates disease pathology in and environmental pesticide model of Parkinson's disease
dc.typeText
dcterms.embargo.expires2023-08-22
dcterms.rights.dplaThe copyright and related rights status of this Item has not been evaluated (https://rightsstatements.org/vocab/CNE/1.0/). Please refer to the organization that has made the Item available for more information.
thesis.degree.disciplineMicrobiology, Immunology, and Pathology
thesis.degree.grantorColorado State University
thesis.degree.levelDoctoral
thesis.degree.nameDoctor of Philosophy (Ph.D.)


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