|Abstract||Alzheimers disease (AD) is characterized by the formation of amyloid-beta (A?) plaques and neurofibrillary tangles; inflammation has been implicated in this process. Our previous work resulted in an animal model of AD-like pathology using the bacterial endotoxin lipopolysaccharide (LPS). Following 7 consecutive injections of LPS, mice have significantly elevated levels of A? with deficits in spatial cognition, but A? levels are decreased following 2 weeks of voluntary exercise. We explored whether exercise could rescue cognitive function and alter microglial phenotypes to decrease A? load. We found that at 2 weeks, there were no cognitive deficits present, but that exercise could enhance performance regardless of previous LPS or saline treatment. These gains were accompanied by modest increases in BDNF, whereas increases in IL-4 mRNA expression were not found. Exercise had no effect on the fluorescence of microglial phenotype marker, arginase, while LPS-administration appeared to increase arginase expression over saline controls.--Abstract.