ArticleGeroScience2019
Lipopolysaccharide exposure in a rat sepsis model results in hippocampal amyloid-β plaque and phosphorylated tau deposition and corresponding behavioral deficits.
Article in GeroScience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 41 citations in OpenAlex.
- Pathological or preventative? Amyloid-β as an effector of innate immunity.Infection and immunity · 2026Review
- Exercise-based modulation of the gut-brain axis: a new direction for neurorehabilitation in Alzheimer's disease.Frontiers in aging neuroscience · 2026Review
- Potentiating Cerebral Perfusion Normalizes Glymphatic Dynamics in Systemic Inflammation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The brain washing system in sepsis-associated encephalopathy.Journal of neuroinflammation · 2025Review
- Region-specific neuroprotective effects of meldonium pretreatment in two models of sepsis-associated encephalopathy.Frontiers in pharmacology · 2025Article
- Cutibacterium Acnes induces Alzheimer's disease-like pathology in brains of wistar rats through structural changes associated with microtubules.Behavioral and brain functions : BBF · 2024Article
- Complementary and alternative medicine on cognitive defects and neuroinflammation after sepsis.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2024Article
- The Interplay between Meningeal Lymphatic Vessels and Neuroinflammation in Neurodegenerative Diseases.Current neuropharmacology · 2024Review
- Morphine aggravates inflammatory, behavioral, and hippocampal structural deficits in septic rats.Scientific reports · 2023Article
- Neurochemical effects of sepsis on the brain.Clinical science (London, England : 1979) · 2023Article
- White matter injury, cholesterol dysmetabolism, and APP/Abeta dysmetabolism interact to produce Alzheimer's disease (AD) neuropathology: A hypothesis and review.Frontiers in aging neuroscience · 2023Article
- Aspirin reverts lipopolysaccharide-induced learning and memory impairment: first evidence from an invertebrate model system.Naunyn-Schmiedeberg's archives of pharmacology · 2022Article
- Sepsis-associated brain injury: underlying mechanisms and potential therapeutic strategies for acute and long-term cognitive impairments.Journal of neuroinflammation · 2022Review
- SIRT3-mediated mitochondrial autophagy in refeeding syndrome-related myocardial injury in sepsis rats.Annals of translational medicine · 2022Article
- Insight Into Regulatory T Cells in Sepsis-Associated Encephalopathy.Frontiers in neurology · 2022Review
- Microglial Priming in Infections and Its Risk to Neurodegenerative Diseases.Frontiers in cellular neuroscience · 2022Review
- Gram-negative bacteria and their lipopolysaccharides in Alzheimer's disease: pathologic roles and therapeutic implications.Translational neurodegeneration · 2021Review
- A binge high sucrose diet provokes systemic and cerebral inflammation in rats without inducing obesity.Scientific reports · 2021Article
- Obesity-induced cognitive impairment in older adults: a microvascular perspective.American journal of physiology. Heart and circulatory physiology · 2021Article
- Interleukin 6 reduces allopregnanolone synthesis in the brain and contributes to age-related cognitive decline in mice.Journal of lipid research · 2020Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Sepsis 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 dentate 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 immunostaining. 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 dentate gyrus. Lipopolysaccharide treatment resulted in behavioral deficits attributable to the dorsal dentate gyrus, including episodic-like memory function that primarily involves spatial, contextual, and temporal orientation and integration. Lipopolysaccharide administration results in hippocampal deposition of amyloid-beta plaques and intracellular phosphorylated tau and results in specific behavioral deficits attributable to the dorsal dentate gyrus. These findings, if persistent, could provide a basis for the higher rate of dementia in longitudinal studies of sepsis survivors.
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Registered trials
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