2026-09-18T19:59:53.618524800Zhttps://opus.uleth.ca/server/oai/request
oai:opus.uleth.ca:10133/65442023-07-26T05:04:55Zcom_10133_3346com_10133_1com_10133_296col_10133_3347col_10133_298
ULethbridge OPUS Repository supervisor Zovoilis, Athanasios author Saville, Luke E. author University of Lethbridge. Faculty of Arts and Science 2023-07-25T19:01:15Z 2023-07-25T19:01:15Z 2023 https://hdl.handle.net/10133/6544 Alzheimer’s disease has a complex etiology and pathology. At the forefront of the disease is the amyloid beta neuropathology where amyloid plaques accumulate as the disease progresses, amidst a state of molecular dysfunction. A relatively understudied component of the molecular pathogenesis underlying Alzheimer’s disease is the potential role of non-coding RNAs as well as their RNA modifications. Here, an integrative molecular and computational approach is used to study the role of non-coding RNAs in the APP NL-G-F Alzheimer’s disease mouse model and human Alzheimer’s disease patients, unveiling that non-coding RNAs transcribed from Short Interspersed Nuclear Elements (SINEs) in mice and humans are aberrantly processed in connection with alterations in gene expression. As well, adenosine to inosine RNA editing is shown to be dysregulated in SINE RNAs and non-coding RNAs involved in protein expression are differentially modified in the hippocampus of APP NL-G-F mice. en non-coding RNAs amyloid beta neuropathology Alzheimer's disease gene expression alterations Role of non-coding RNAs in amyloid beta neuropathology and Alzheimer's disease Thesis 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