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Please use this identifier to cite or link to this item: http://hdl.handle.net/11375/24260
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DC FieldValueLanguage
dc.contributor.advisorSingh, Gurmit-
dc.contributor.authorMcKay, Margaret-
dc.date.accessioned2019-04-26T12:50:43Z-
dc.date.available2019-04-26T12:50:43Z-
dc.date.issued1995-03-
dc.identifier.urihttp://hdl.handle.net/11375/24260-
dc.description.abstractMitochondria are intracellular organelles responsible for oxidative phosphorylation. They contain their own DNA which encodes some components involved in oxidative phosphorylation. Mitochondrial DNA is very susceptible to mutations. Mitochondrial abnormalities have been observed in several disorders of muscle and brain. Alzheimer's disease is a form of dementia characterized by the formation of numerous neuritic plaques and neurofibrillary tangles. There is evidence suggesting a possible role for mitochondrial abnormalities in Alzheimer's disease. The goal of this project was to determine if there were quantitative changes in mitochondrial DNA content in large neurons from Alzheimer's disease patients, compared to age-matched control patients. The relative mitochondrial DNA content per unit area was assessed in brain sections from Alzheimer's disease subjects and age-matched control subjects using in situ hybridization to mitochondrial DNA. The results were not conclusive due to technical concerns with the in situ hybridization technique which are discussed.en_US
dc.language.isoenen_US
dc.subjectmitochondrial DNAen_US
dc.subjectalzheimer's diseaseen_US
dc.subjectDNAen_US
dc.subjectin situ hybridizationen_US
dc.titleMitochondrial DNA in Alzheimer's Disease: Examination using In Situ Hybridizationen_US
dc.title.alternativeMitochondrial DNA in Alzheimer's Diseaseen_US
dc.typeThesisen_US
dc.contributor.departmentBiochemistryen_US
dc.description.degreetypeThesisen_US
dc.description.degreeMaster of Science (MS)en_US
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