Preventive effects of multisensory rehabilitation on development of cognitive dysfunction following systemic inflammation in aged rats

Abstract

Systemic inflammation can trigger transient or longer-lasting cognitive impairments, particularly in elderly patients. However, its pathogenesis has not been sufficiently clarified. In this study, we explored the potential effects of multisensory rehabilitation on cognitive dysfunction following systemic inflammation using an animal model. Aged male Wister rats were randomly injected intraperitoneally with either saline (control) or lipopolysaccharide (LPS; 5 mg/kg). After injection, both groups of rats were randomly assigned to either of two housing conditions (n = 8 in each condition): a standard cage environment (SC group) or a multisensory early rehabilitation environment (ER group). Cognitive function was examined after 7 days in the assigned environmental condition using a novel object recognition test. In the SC group, the LPS-treated rats showed impaired cognitive function compared with the control animals. These memory deficits were positively correlated with the levels of both tumor necrosis factor (TNF)-α and interleukin (IL)-1β in the hippocampus. On the other hand, in the LPS-treated ER group, neither cognitive impairment nor an increase in hippocampal levels of both TNF-α and IL-1β was found. These results imply that early rehabilitation (ER) intervention may be effective in preventing cognitive dysfunction following systemic inflammation via its anti-neuroinflammatory effects.

A noradrenergic lesion aggravates the effects of systemic inflammation on the hippocampus of aged rats

“…In the long-term group, cytokine and chemokine levels in LPS-treated and DSP4+LPS-treated rats were returned to control levels, suggesting a resolution of inflammation after seven days. While previous studies showed increased hippocampal IL-1β levels after LPS exposure in rats [ 65 , 66 ], this was not the case under our experimental conditions, possibly due to differences in animal models or incubation period between LPS administration and sample collection. It is also noteworthy that the LPS dose used in our study (0.75 mg/kg) was lower than the ones used in the Fu et al [ 65 ] (2 mg/kg) and Kawano et al [ 66 ] (5 mg/kg) studies.…”

“…While previous studies showed increased hippocampal IL-1β levels after LPS exposure in rats [ 65 , 66 ], this was not the case under our experimental conditions, possibly due to differences in animal models or incubation period between LPS administration and sample collection. It is also noteworthy that the LPS dose used in our study (0.75 mg/kg) was lower than the ones used in the Fu et al [ 65 ] (2 mg/kg) and Kawano et al [ 66 ] (5 mg/kg) studies. However, we found that the NE lesion caused by the DSP4 toxin resulted in significantly elevated hippocampal IL-1β levels 4 hours after the LPS administration.…”

Changes in Gene Expression and Neuroinflammation in the Hippocampus after Focal Brain Ischemia: Involvement in the Long-Term Cognitive and Mental Disorders

“…Studies in rodents have shown that attenuation of neuroinflammation in the hip pocampus after MCAO, for example, by exposure of ani mals to an enriched environment [40] or administration of insulin like growth factor 1 [41] improves ischemia induced cognitive deficits. On the contrary, activation of neuroinflammation by LPS resulted in memory loss, which was observed seven days [42] and even ten months [43] after a single administration of endotoxin, and reli ably correlated with the increased levels of the pro inflammatory cytokines TNF α and IL 1β in the hip pocampus.…”

Management of cognition as reported in Japanese historical documents and modern anesthesiology research papers

“…Five presenters presented their own most recent research outcomes and reviewed related publications. Takashi Kawano explained that postoperative delirium and POCD are closely related, and both are the result of an inflammatory reaction in the nervous system [28,29]. He also reported that postoperative pain management and intensive early rehabilitation seem to be important for the prevention of POCD in elderly patients.…”