Lipopolysaccharide (LPS), a bacterial endotoxin that has been widely used in experimental neuroscience to model neuroinflammation and its effects on cognitive functions. This study investigates the dose-dependent impact of LPS-induced neurotoxicity on memory processing and alertness in Wistar rats. 20 Wistar rats were randomly divided into four groups: Control, Low-Dose LPS, Medium-Dose LPS, and High-Dose LPS. The animals underwent behavioral assessments using the Barnes Maze, Object Recognition Test (ORT), and Navigational Maze to evaluate memory and alertness. Results indicated that increasing LPS doses led to a progressive decline in memory performance and alertness. The Barnes Maze test showed that spatial learning and memory retention were significantly impaired in the Medium and High-Dose groups compared to controls. The Object Recognition Test revealed that discrimination indices decreased in a dose-dependent manner, indicating deficits in object recognition memory. Similarly, the Navigational Maze test demonstrated reduced exploratory activity and longer escape latencies in LPS-treated rats, suggesting compromised alertness. Biochemical analyses showed elevated levels of nitric oxide (NO) and interleukin-6 (IL-6) in brain tissues of LPS-treated rats, correlating with cognitive impairments. Histopathological examination of the hippocampus revealed neuronal damage, with the highest degree of neurodegeneration observed in the High-Dose LPS group. These findings suggest that LPS-induced neurotoxicity disrupts cognitive functions in a dose-dependent manner, with higher doses exacerbating memory and alertness deficits. The results contribute to understanding the role of neuroinflammation in cognitive decline and provide insights into potential therapeutic strategies for neurodegenerative diseases characterized by chronic inflammation, such as Alzheimer's disease.
Ajah et al. (Mon,) studied this question.