ArticleBrain and behavior2020
Lipopolysaccharide exposure during late embryogenesis triggers and drives Alzheimer-like behavioral and neuropathological changes in CD-1 mice.
Article in Brain and behavior, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 14 citations in OpenAlex.
- Maternal Immune Activation Leads to Lasting Sex-Specific Changes in Behavior and Hippocampal Morphological and Molecular Features in 12-Month-Old Rat Offspring.International journal of molecular sciences · 2026Article
- The Role of Prenatal Microglial Activation and Its Sex Differences in the Development of Neuropsychiatric Disorders and Neurodegenerative Diseases.International journal of molecular sciences · 2025Review
- The Interplay of Inflammation and Gut-Microbiota Dysbiosis in Alzheimer's Disease: Mechanisms and Therapeutic Potential.International journal of molecular sciences · 2025Review
- The Inflammation-Induced Dysregulation of Reelin Homeostasis Hypothesis of Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2024Review
- Small molecule targeting long noncoding RNA GAS5 administered intranasally improves neuronal insulin signaling and decreases neuroinflammation in an aged mouse model.Scientific reports · 2023Article
- Evaluation of dihydrotestosterone and dihydroprogesterone levels and gene expression of genes involved in neurosteroidogenesis in the SH-SY5Y Alzheimer disease cell model.Frontiers in neuroscience · 2023Article
- Resveratrol ameliorates maternal immune activation-associated cognitive impairment in adult male offspring by relieving inflammation and improving synaptic dysfunction.Frontiers in behavioral neuroscience · 2023Article
- Microglial Priming in Infections and Its Risk to Neurodegenerative Diseases.Frontiers in cellular neuroscience · 2022Review
- Prenatal exposure to inflammation increases anxiety-like behaviors in F1 and F2 generations: possible links to decreased FABP7 in hippocampus.Frontiers in behavioral neuroscience · 2022Article
- Environmental enrichment improves declined cognition induced by prenatal inflammatory exposure in aged CD-1 mice: Role of NGPF2 and PSD-95.Frontiers in aging neuroscience · 2022Article
- The Impact of Systemic Inflammation on Alzheimer's Disease Pathology.Frontiers in immunology · 2021Review
- Ellagic Acid Inhibits Neuroinflammation and Cognitive Impairment Induced by Lipopolysaccharides.Neurochemical research · 2020Article
- Lipopolysaccharide exposure during late embryogenesis triggers and drives Alzheimer-like behavioral and neuropathological changes in CD-1 mice.Brain and behavior · 2020Article
- Effects of Embryonic Inflammation and Adolescent Psychosocial Environment on Cognition and Hippocampal Staufen in Middle-Aged Mice.Frontiers in aging neuroscience · 2020Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
introductionInfections could contribute to Alzheimer's disease (AD) neuropathology in human. However, experimental evidence for a causal relationship between infections during the prenatal phase and the onset of AD is lacking.
methodsCD-1 mothers were intraperitoneally received lipopolysaccharide (LPS) with two doses (25 and 50 μg/kg) or normal saline every day during gestational days 15-17. A battery of behavioral tasks was used to assess the species-typical behavior, sensorimotor capacity, anxiety, locomotor activity, recognition memory, and spatial learning and memory in 1-, 6-, 12-, 18-, and 22-month-old offspring mice. An immunohistochemical technology was performed to detect neuropathological indicators consisting of amyloid-β (Aβ), phosphorylated tau (p-tau), and glial fibrillary acidic protein (GFAP) in the hippocampus.
resultsCompared to the same-aged controls, LPS-treated offspring had similar behavioral abilities and the levels of Aβ42, p-tau, and GFAP at 1 and 6 months old. From 12 months onward, LPS-treated offspring gradually showed decreased species-typical behavior, sensorimotor ability, locomotor activity, recognition memory, and spatial learning and memory, and increased anxieties and the levels of Aβ42, p-tau, and GFAP relative to the same-aged controls. Moreover, this damage effect (especially cognitive decline) persistently progressed onwards. The changes in these neuropathological indicators significantly correlated with impaired spatial learning and memory.
conclusionsPrenatal exposure to low doses of LPS caused AD-related features including behavioral and neuropathological changes from midlife to senectitude.
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