| Abstract | Alzheimer's Disease (AD) is a neurodegenerative disease that is characterized by deficits in learning and memory. In AD, Amyloid-Beta (AB) is over-produced and accumulates in the brain forming plaques. This extracellular deposition of AB interferes with normal neuronal synapse activity leading to neuronal dysfunction and degeneration. Lipopolysaccharide (LPS), a component of gram-negative bacteria, has previously been shown to induce an inflammatory response that increases AB found in the brain. Dendritic spines are protrusions on the dendrites of neurons that exhibit plasticity depending on outside stimuli. This plasticity is heavily correlated to learning and memory. Likewise, the quantity of these spines is correlated with the number of functioning synapses on the neuron. The purpose of this study was to investigate how LPS-induced inflammation would affect dendritic spine density of hippocampal neurons. LPS was administered and dendritic spine density was quantified. There was not a significant difference in dendritic spine density following LPS treatment when compared to saline controls. The loss of dendritic spines occurs early on in AD development making it an important target for early intervention in AD. Future studies should further investigate the relationships between inflammation, AB, and functional synapses. |
