| dc.description.abstract | Alzheimer's Disease (AD) is a progressive neurodegenerative disorder characterized by memory loss and cognitive decline. AD pathologies include neurofibrillary tangles, amyloid--beta plaques (A-beta), and neuronal cell death. Our lab has previously shown that systemic inflammation in mice, resulting from 7 days of LPS injections, led to cognitive deficits as well as increased A-beta levels in the CNS. Interestingly, exercise was shown by our lab to decrease A-beta levels in mice treated with LPS to levels equal to those of control mice. This identified exercise as a possible therapeutic treatment for AD, but the mechanism for this effect is currently unknown. We identified microglia as one possible cell responsible for the decrease in A-beta. Microglia are the immune cells of the brain, with functions including secretion of pro-inflammatory cytokines, release of growth factors, and phagocytosis of debris. Microglia are activated by both inflammation and exercise. We hypothesized that exercise would increase the number of activated microglia in the CNS. We found that following LPS-administration animals in both the sedentary and exercise groups had increased levels of activated microglia, compared to saline-administered animals, but did not differ from each other. Interestingly, animals that had been injected with saline, followed by two weeks of voluntary exercise, displayed more activated microglia than those in the sedentary recovery group (p = 0.07). This suggests that exercise may play a role in activating microglia if not previously primed by inflammation. Activated microglia can be oriented either towards a neuroprotective or a neurodegenerative phenotype, and we suggest further studies should be performed, identifying whether exercise alters these phenotypes. Understanding the role microglia and exercise play in the removal of A-beta from the CNS, may lead to changes in AD treatments. | |
