| dc.description.abstract | Alzheimer'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-beta. Prior research in animal models has pointed to soluble A-beta causing synaptic disruption. In the present study, the aim was to understand the effect that A-beta has on synapses. We used immunolabeling in an AD transgenic mouse model. The 5xFAD mouse model utilized in this study rapidly develops A-beta 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-beta in order to visualize the amount of A-beta 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-beta accumulation affects the observed number of synapses in the hippocampus. | |
