| Emerging research on neurodegenerative diseases, such as Alzheimer's disease (AD), has tentatively implicated inflammatory processes in the progression of the disease and its clinical manifestations. Previously our lab has explored this link between AD and inflammation. We established a non-transgenic animal model of acute inflammation that produces Aβ peptide in a purportedly similar fashion to early sporadic AD, showing that peripheral administration of the endotoxin lipopolysaccharide (LPS), a component of the cell wall of gram-negative bacteria, leads to elevated hippocampal Aβ and cognitive deficits. Interestingly, while investigating these peripheral inflammatory connections to AD, data suggested that animals that swam as part of a 9-day behavioral paradigm have reduced hippocampal Aβ levels. In the present study we sought to explore the impact of exercise on the cognitive deficits and Aβ peptide load seen in our inflammatory model. We hypothesized that voluntary exercise would reduce Aβ protein volume in the hippocampus and reduce cognitive impairment after administration of LPS. Our results indicate that mice allowed voluntary exercise (running wheel) for seven days following 7 consecutive days of a single LPS injection displayed reduced hippocampal Aβ levels compared to sedentary controls with no differences in behavior between groups. |
