Research Paper Volume 13, Issue 18 pp 22092—22108
Adulthood systemic inflammation accelerates the trajectory of age-related cognitive decline
- 1 Department of Neuroscience, McKnight Brain Institute, University of Florida, Gainesville, FL 32610, USA
- 2 Genetics and Genomics Program, University of Florida, Gainesville, FL 32611, USA
Received: August 13, 2021 Accepted: September 20, 2021 Published: September 29, 2021https://doi.org/10.18632/aging.203588
How to Cite
Copyright: © 2021 Barter et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
In order to understand the long-term effects of systemic inflammation, it is important to distinguish inflammation-induced changes in baseline cognitive function from changes that interact with aging to influence the trajectory of cognitive decline. Lipopolysaccharide (LPS; 1 mg/kg) or vehicle was administered to young adult (6 months) male rats via intraperitoneal injections, once a week for 7 weeks. Longitudinal effects on cognitive decline were examined 6 and 12 months after the initial injections. Repeated LPS treatment, in adults, resulted in a long-term impairment in memory, examined in aged animals (age 18 months), but not in middle-age (age 12 months). At 12 months following injections, LPS treatment was associated with a decrease in N-methyl-D-aspartate receptor-mediated component of synaptic transmission and altered expression of genes linked to the synapse and to regulation of the response to inflammatory signals. The results of the current study suggest that the history of systemic inflammation is one component of environmental factors that contribute to the resilience or susceptibility to age-related brain changes and associated trajectory of cognitive decline.