| dc.description.abstract | Alzheimer's disease is currently the sixth leading cause of death in the United States, affecting an estimated 5.1 million Americans. This disease is characterized by amyloid-beta plaques and neurofibrillary tangles, which both lead to impaired neuron communication contributing to memory loss, disorientation, and eventually difficulty speaking and swallowing. Exact mechanisms leading to the development or treatment of AD are not well understood, but certain factors, such as chronic inflammation, are known to expedite onset and progression. That said, previous work from our laboratory showed that following an immune challenge, exercise led to decreased levels of amyloid-beta in mice. From this knowledge, this project was designed to determine specifically why exercise contributed to improved AD pathology in the hilus and subiculum, regions of the brain particularly susceptible to damage that are critical for learning and memory. We hypothesized that one week of exercise in mice would lead to a switch in phenotype of microglial cells, the resident immune cells of the brain, from pro-inflammatory to anti-inflammatory. If this were the case, there would be increased expression of Arg-1, a marker for the anti-inflammatory phenotype of microglial cells. However, results did not show a significant difference in Arg-1 expression across treatment groups. Future studies could increase the amount of inflammation induced, use a wider variety of cell markers to better account for the diverse phenotypes microglial cells can possess, or explore another mechanism by which exercise reduces inflammation. | |
