| Abstract | Alzheimer's disease (AD) is a neurodegenerative disorder that affects over 5 million Americans, and there is currently no cure. AD is characterized by A-beta plaques, neurofibrillary tangles, inflammation, and neuronal/ synapse loss in the brain. Oligomeric A-beta has been hypothesized to bind to receptors in neuronal synapses, thus disrupting synapse signaling. Neuroscientists are trying to determine if the synapse disruption caused by A-beta leads to the cognitive dysfunction seen in AD. The present studies goal is to determine if A-beta is responsible for the decrease in synaptic density in the CA1 region of the hippocampus in mice. To quantify synaptic density the present study will count the number of dendritic spines on neurons. The study utilized a tissue clearing technique, which removed lipids from the brain and eliminated light scatter due to these fatty acids. I expect the tissue clearing technique to result in enhanced resolution of the images of the neurons. This study will also determine if 5xFAD+, an AD transgenic mouse model, mice have fewer dendritic spines in comparison to Wild Type (WT) mice. I expect there to be a decrease in the number of observed dendritic spines in the 5xFAD+ mice compared to the control group. |
