Abstract
Neuroinflammation has been known to play a critical role in the pathogenesis of Alzheimer’s disease (AD) through amyloidogenesis. However, it is not yet clear whether intraperitoneal (i.p.) injection of lipopolysacchride (LPS) is sufficient for inducing AD model. In this present study, we investigated the amyloidogenic and memorial dysfunctional effects by differential dosages and duration of injected LPS in different aged mice, and acceleration effect of LPS on the amyloidogenesis and memory dysfunction in Tg2576 mice. We found that i.p. injection of LPS at both doses (0.25 and 0.75 mg/kg/day, 7 times) could induce memory dysfunction and amyloidogenesis, but did not show significant difference between two doses. In addition, LPS-injection to three ages (4, 6 and 10 weeks old) of mice revealed memory decline and amyloidogenic effect in the age-dependent manner. To define LPS-induced elevation on memory and amyloidogenesis, we injected LPS (0.25 mg/kg/day, 7 times) to APP over-expressing Tg2576 mice and found that systemic injection of LPS also accelerated memory decline and amyloidogenesis in AD model mice. Therefore, this study showed that LPS-induced memory dysfunction and amyloidogenesis was sufficient through 7 times injection of 0.25 mg/kg/day, and 10 or more weeks old mice were sufficient. In addition, we confirmed LPS-induced acceleration of amyloidogenesis in APP-overexpressing mice, suggests that systemic injection of LPS might be a useful method for neuroinflammation-associated AD.
