Just like how a rock thrown into a pond creates ripples that disturb the calm surface, inflammatory stress can disrupt the intricate network of connections in the aging brain. A recent study examined how exposure to inflammation affects the default mode network (DMN), which is responsible for our spontaneous cognitive function. In the study, aged male rats were injected with lipopolysaccharide (LPS) to induce inflammation, while others received saline injections as controls. The rats’ cognitive functions were assessed using a maze test, and their brains were scanned using resting-state functional magnetic resonance imaging (rs-fMRI) to analyze the DMN’s functional connectivity (FC) and topology structures. The results showed that the LPS-exposed rats experienced short- and long-term impairments in learning and spatial memory. Additionally, graph theory analysis of the rs-fMRI data revealed changes in DMN connectivity and topology structures over time. Interestingly, alterations in FC lasted for both short- and long-term, while changes in topology structures were only observed in the early stage. These findings suggest that inflammatory stress has prolonged effects on the connectivity of the aging brain, providing valuable insights into the underlying mechanisms of cognitive dysfunction. If you’re curious about how inflammation affects our brains as we age, dive into the full research article for more!

Inflammatory stress in anesthesia management and surgical process has been reported to induce long-term cognitive dysfunction in vulnerable aged brain, while few studies focused on the network mechanism. The default mode network (DMN) plays a significant role in spontaneous cognitive function. Changes in topology structure and functional connectivity (FC) of DMN in vulnerable aged brain following inflammatory stress-induced long-term cognitive dysfunction are rarely studied. Eighty-eight aged male rats received intraperitoneal injection of lipopolysaccharide (LPS) as treatment or equal amount of normal saline (NS) as control. Morris Water Maze (MWM) was performed to assess short- (<7 days) and long-term (>30 days) learning and spatial working memory. Enzyme-linked immunosorbent assay (ELISA) was used to measure systemic and hippocampus inflammatory cytokines. Real-time polymerase chain reaction (RT-PCR) was used to measure the changes in gene level. Resting-state functional magnetic resonance imaging (rs-fMRI) was used to exam brain function prior to MWM on days 3, 7, and 31 after LPS exposure. Graph theory analysis was used to analyze FC and topology structures in aged rat DMN. Aged rats treated with LPS showed short- and long-term impairment in learning and spatial working memory in MWM test. Graph theory analysis showed temporary DMN intrinsic connectivity increased on day 3 followed with subsequent DMN intrinsic connectivity significantly altered on day 7 and day 31 in LPS-exposed rats as compared with controls. Short- and long-term alterations were observed in FC, while alterations in topology structures were only observed on day 3. Rats with inflammatory stress exposure may cause short- and long-term alterations in intrinsic connectivity in aged rat’s DMN while the changes in topology structures only lasted for 3 days. Inflammatory stress has prolonged effects on FC, but not topology structures in venerable aged brain.

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