Interruption of neuron-microglia bidirectional communication to modulate cofilin:actin rod formation
| dc.contributor.author | Zoller, Maia, author | |
| dc.contributor.author | Bamburg, James, advisor | |
| dc.contributor.author | Chanda, Soham, committee member | |
| dc.contributor.author | Zabel, Mark, committee member | |
| dc.date.accessioned | 2022-05-30T10:21:49Z | |
| dc.date.available | 2022-05-30T10:21:49Z | |
| dc.date.issued | 2022 | |
| dc.description.abstract | Immune responses in the central nervous system are mediated by microglia, whose responses to CNS threats can be replicated in vitro to study the role of microglia in the onset, progression, and treatment of neurodegenerative diseases. Previous work has identified a pathway common to neurodegenerative diseases such as Alzheimer's Disease, Parkinson's Disease, and HIV-Associated Neurocognitive Dementia in which the actin-severing protein, cofilin, forms a 1:1 bundle with actin making rod-shaped inclusions (rods) that can be found in the dendrites and axons of neuronal cells. This thesis focuses on developing methods for examining the role of primary microglia, activated by different factors, to secrete rod-inducing chemokines/cytokines or directly attacking neurons leading to neuronal death. Understanding both of these mechanisms is important in study of neuroinflammation and disease progression. Hemin, a hemoglobin metabolite, and alarmin, S100B, a astrocyte secreted, calcium binding protein, protein, were used to model the environment of intracerebral hemorrhage and general neuroinflammation respectively. Preliminary experimental results suggest blockage of actin-rod inducing signaling pathways via CXCR4/CCR5 receptor antagonist improves neuronal survival to both microglia conditioned medium and direct exposure the microglia-activating hemin or S100B. Further studies are in progress to obtain sufficient statistical data to verify these results. | |
| dc.format.medium | born digital | |
| dc.format.medium | masters theses | |
| dc.identifier | Zoller_colostate_0053N_17224.pdf | |
| dc.identifier.uri | https://hdl.handle.net/10217/235254 | |
| dc.language | English | |
| dc.language.iso | eng | |
| dc.publisher | Colorado State University. Libraries | |
| dc.relation.ispartof | 2020- | |
| dc.rights | Copyright and other restrictions may apply. User is responsible for compliance with all applicable laws. For information about copyright law, please see https://libguides.colostate.edu/copyright. | |
| dc.subject | chemokines | |
| dc.subject | CXCR4 | |
| dc.subject | neuroinflammation | |
| dc.subject | cofilin:actin rods | |
| dc.subject | Alzheimer's disease | |
| dc.subject | microglia | |
| dc.title | Interruption of neuron-microglia bidirectional communication to modulate cofilin:actin rod formation | |
| dc.type | Text | |
| dcterms.rights.dpla | This Item is protected by copyright and/or related rights (https://rightsstatements.org/vocab/InC/1.0/). You are free to use this Item in any way that is permitted by the copyright and related rights legislation that applies to your use. For other uses you need to obtain permission from the rights-holder(s). | |
| thesis.degree.discipline | Biochemistry and Molecular Biology | |
| thesis.degree.grantor | Colorado State University | |
| thesis.degree.level | Masters | |
| thesis.degree.name | Master of Science (M.S.) |
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