Date of Award
Senior Honors Thesis
College or School
Biological Sciences; Molecular, Cellular, & Biomedical Sciences
Program or Major
Neuroscience & Behavior and Biomedical Sciences: Medical Microbiology
Bachelor of Science
Alzheimer’s Disease (AD) is a neurodegenerative condition caused by the abnormal accumulation of amyloid β plaque. While small amounts of amyloid β plaque is to be expected with increased age, AD presents amyloid precursor protein (APP), a gene promoting inappropriate plaque formation, causing early neuronal death and tissue depreciation. APP23 transgenic mouse models contain the human mutation in the neocortical and hippocampal positions, areas revealing of plaque accumulation and memory loss. Within the hippocampal cortices, the primary cilia, which regulate higher cognition and neurodevelopment can be studied along with burst suppressions, or moments of high focal activity, to target potential early biomarkers for progressive neurodegeneration by utilizing EEG/EMG recordings, immunohistochemistry, and confocal microscopy. It was hypothesized that the younger APP23 mice establish the connection between stimuli better than the wildtype mice. Under trace fear conditioning, if more burst suppressions are present for APP23 mice, then their genotype is more successful than the control. In early development, the transgenic mice show to have more active neurons and, therefore, are more intelligent than the control. The APP mouse showed more significant burst suppressions after the tone stimuli prior to the time of the shock compared to the control. Indicative of a learning response, the transgenic subject displayed apprehension to the external stimuli whereas the wildtype mice did not yet make the connection.
Walsh, Sierra Rose Mae, "Neuronal Primary Cilia in Postnatal Brains & Alzheimer’s Disease Mice EEG Patterns Under Fear Conditioning" (2023). Honors Theses and Capstones. 752.