Genetic Modulation of β-Amyloid Neurotoxicity and Protection by Nicotinic Agents
dc.contributor.advisor | Basu, Alakananda | |
dc.contributor.committeeMember | Forster, Michael | |
dc.contributor.committeeMember | Singh, Meharvan | |
dc.creator | Martin, Shelley E. | |
dc.date.accessioned | 2019-08-22T21:34:09Z | |
dc.date.available | 2019-08-22T21:34:09Z | |
dc.date.issued | 2007-05-01 | |
dc.date.submitted | 2014-02-24T14:54:05-08:00 | |
dc.description.abstract | Martin, Shelley E., Genetic Modulation of β-Amyloid Neurotoxicity and Protection by Nicotinic Agents. Master of Science (Pharmacology and Neuroscience), May, 2007, 53 pp., 7 figures, 2 tables, bibliography, 95 titles. Β-amyloid1-42 (Aβ42) has been implicated in the pathogenesis of Alzheimer’s disease (AD); however, the amount of this peptide in the brain does not correlate well with the presence or severity of AD. This project tested the hypothesis that individual differences exist in susceptibility to Aβ42 neurotoxicity arising from the differences in the expression of α7 nicotinic acetylcholine receptors α7 nACHRs). This hypothesis was tested in primary neuronal cultures derived from inbred mouse strains which differ in expression of α7 nAChRs. Also, the ability of nicotinic agents to modulate Aβ42 toxicity was examined. Significant strain differences in susceptibility to Aβ42 toxicity were found; however, these were not related to levels of α7 nAChRs. Additionally, strain differences were found in the ability of α7-selective partial agonist, an α7-selective antagonist and a α4β2 nAChR-selective antagonist to protect against this toxicity. Inbred strains of mice may be useful in uncovering the pathophysiology of AD. | |
dc.format.mimetype | application/pdf | |
dc.identifier.uri | https://hdl.handle.net/20.500.12503/29429 | |
dc.language.iso | en | |
dc.provenance.legacyDownloads | 1 | |
dc.subject | Life Sciences | |
dc.subject | Medical Neurobiology | |
dc.subject | Medical Pharmacology | |
dc.subject | Medicine and Health Sciences | |
dc.subject | Nervous System Diseases | |
dc.subject | Neuroscience and Neurobiology | |
dc.subject | Other Neuroscience and Neurobiology | |
dc.subject | Pharmacology | |
dc.subject | Genetic modulation | |
dc.subject | β-amyloid neurotoxicity | |
dc.subject | beta-amyloid neurotoxicity | |
dc.subject | nicotinic agents | |
dc.subject | protection | |
dc.subject | Aβ42 | |
dc.subject | Alzheimer’s Disease | |
dc.subject | peptide | |
dc.subject | α7 nicotinic acetylcholine | |
dc.subject | nAChRs | |
dc.subject | mice | |
dc.subject | pathophysiology | |
dc.title | Genetic Modulation of β-Amyloid Neurotoxicity and Protection by Nicotinic Agents | |
dc.type | Thesis | |
dc.type.material | text | |
thesis.degree.department | Graduate School of Biomedical Sciences | |
thesis.degree.discipline | Pharmacology and Neuroscience | |
thesis.degree.grantor | University of North Texas Health Science Center at Fort Worth | |
thesis.degree.name | Master of Science |
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