Lipopolysaccharide exposure in a rat sepsis model results in hippocampal amyloid- β plaque and phosphorylated tau deposition and corresponding behavioral deficits

AbstractSepsis is a severe systemic inflammatory response to infection associated with acute and chronic neurocognitive consequences, including an increased risk of later-life dementia. In a lipopolysaccharide-induced rat sepsis model, we have demonstrated neuroinflammation, cortical amyloid-beta plaque deposition, and increased whole brain levels of phosphorylated tau. Hippocampal abnormalities, particularly those of the dentate gyrus, are seen in Alzheimer ’s disease and age-related memory loss. The focus of this study was to determine whether Aβ plaques and phosphorylated tau aggregates occur in the hippocampus as a consequence of lipopolysaccharide administration, and whether behavioral abnormalities related to the hippocampus, particularly the d entate gyrus, can be demonstrated. Male Sprague Dawley rats received an intraperitoneal injection of 10 mg/kg of lipopolysaccharide endotoxin. Control animals received a saline injection. Seven days post injection, Aβ plaques and phosphorylated tau in the hippocampus were quantified following immu nostaining. Behavioral tests that have previously been shown to result in specific deficits in dentate gyrus-lesioned rats were administered. Lipopolysaccharide treatment results in the deposition of beta amyloid plaques and intracellular phosphorylated tau in the hippocampus, including the dorsal d entate gyrus. Lipopolysaccharide treatment resulted in behavioral deficits attributable to the dorsal dentate gyrus, including episodi...

Source: AGE - August 30, 2019 Category: Geriatrics Source Type: research