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dc.contributor.authorFrediani, Gabrielle
dc.date.accessioned2019-09-25T20:41:26Z
dc.date.available2019-09-25T20:41:26Z
dc.date.issued2019-05-19
dc.identifier.urihttps://repository.tcu.edu/handle/116099117/27016
dc.description.abstractAlzheimer?s disease (AD) is a neurodegenerative disease that leads to cognitive deficits. The brain dysfunction in AD is marked by an increase in amyloid-beta, the protein responsible for plaque deposition in the brain. The severity of the cognitive deficits positively correlates with the load of A?. Prior research in animal models has pointed to soluble A? causing synaptic disruption. In the present study, the aim was to understand the effect that A? has on synapses. We used immunolabeling in an AD transgenic mouse model. The 5xFAD mouse model utilized in this study rapidly develops A? pathology. This model mimics the pathophysiology of AD in humans. The mouse model used was also knock-in transgenic for Green Fluorescent Protein (GFP) on mature CNS neurons. Using immunolabeling, GFP was tagged with antibodies, thus making neurons visible under the microscope. Antibodies were also used for A? in order to visualize the amount of A? protein and its location. Images of synapses were obtained in both FAD+/GFP+ and FAD-/GFP+ mice. Comparing these images, we were able to determine that A? accumulation affects the observed number of synapses in the hippocampus.
dc.subjectamyloid beta
dc.subjectdendritic spines
dc.titleThe Effect of Amyloid Beta on Synapses
etd.degree.departmentBiology


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