ArticleHeliyon2024
Mitochondrial dysfunction precedes hippocampal IL-1β transcription and cognitive impairments after low-dose lipopolysaccharide injection in aged mice.
Article in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- Brain mitochondria as key drivers of cognition and behaviour.Nature reviews. Neuroscience · 2026Review
- Mitochondrial transplantation for delirium superimposed on dementia: from pathogenic mechanisms to clinical translation challenges.Frontiers in aging neuroscience · 2026Review
- Neuroinflammatory stress preferentially impacts synaptic MAPK signaling and mitochondria in excitatory neurons.Molecular neurodegeneration advances · 2026Article
- ATF5-Dependent GDF15 Expression Mediates Anesthesia-Induced Neuroprotection Against Stroke.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Integrating network pharmacology and experimental validation deciphers the improving effect and mechanisms of Shenwu Yizhi capsule on cognitive impairment in vascular dementia rats.Metabolic brain disease · 2025Article
- Laparotomy and burst suppression-inducing sevoflurane induce subtle long-term changes in anxiety and social behavior in late postnatal mice.Korean journal of anesthesiology · 2025Article
- Revisiting anesthesia-induced preconditioning for neuroprotection in the aging brain: a narrative review.Korean journal of anesthesiology · 2025Review
- Global Trends and Collaborative Networks in Crush Syndrome: A Bibliometric Analysis From 2000 to 2025.Journal of multidisciplinary healthcare · 2025Article
- Histopathological Analysis of Lipopolysaccharide-Induced Liver Inflammation and Thrombus Formation in Mice: The Protective Effects of Aspirin.Current issues in molecular biology · 2024Article
- Article
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute cognitive impairments termed delirium often occur after inflammatory insults in elderly patients. While previous preclinical studies suggest mitochondria as a target for reducing neuroinflammation and cognitive impairments after LPS injection, fewer studies have evaluated the effects of a low-grade systemic inflammation in the aged brain. Thus, to identify the significance of mitochondrial dysfunction after a clinically relevant systemic inflammatory stimulus, we injected old-aged mice (18-20 months) with low-dose lipopolysaccharide (LPS, 0.04 mg/kg). LPS injection reduced mitochondrial respiration in the hippocampus 24 h after injection (respiratory control ratio [RCR], state3u/state4o; control = 2.82 ± 0.19, LPS = 2.57 ± 0.08). However, gene expression of the pro-inflammatory cytokine IL-1β was increased (RT-PCR, control = 1.00 ± 0.30; LPS = 2.01 ± 0.67) at a more delayed time point, 48 h after LPS injection. Such changes were associated with cognitive impairments in the Barnes maze and fear chamber tests. Notably, young mice were unaffected by low-dose LPS, suggesting that mitochondrial dysfunction precedes neuroinflammation and cognitive decline in elderly patients following a low-grade systemic insult. Our findings highlight mitochondria as a potential therapeutic target for reducing delirium in elderly patients.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.