ArticleMolecular neurobiology2014
Acute brain inflammation and oxidative damage are related to long-term cognitive deficits and markers of neurodegeneration in sepsis-survivor rats.
Article in Molecular neurobiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 2 of them syntheses that pooled it.
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Who cites it
47 citing papers in PubMed, 2 syntheses or guidelines pooled it, 88 citations in OpenAlex.
- A systematic review of the therapeutic potential of nicotinamide adenine dinucleotide precursors for cognitive diseases in preclinical rodent models.BMC neuroscience · 2025Pooled it
- Long-Term Cognitive Outcomes After Sepsis: a Translational Systematic Review.Molecular neurobiology · 2019Pooled it
- Effects of Lactate on Improving Cognitive Function and Survival Rate in a Mouse Model of Post-Sepsis Cognitive Impairment.Actas espanolas de psiquiatria · 2026Article
- Hyperbaric oxygen therapy in sepsis-associated encephalopathy: pathophysiological rationale, preclinical evidence, and translational challenges.Frontiers in cellular neuroscience · 2026Review
- Molecular insights into irisin's role in the regulation of programmed cell death: mechanisms and therapeutic potential.Journal of molecular medicine (Berlin, Germany) · 2025Review
- Integrated multi omics and machine learning reveal mitochondrial immunometabolic networks in sepsis associated encephalopathy.Scientific reports · 2025Article
- Biomarkers of sepsis associated encephalopathy: a bibliometric and visualized analysis.Frontiers in neurology · 2025Article
- Sepsis-associated encephalopathy: Autophagy and miRNAs regulate microglial activation.Physiological reports · 2024Review
- CD137L Inhibition Ameliorates Hippocampal Neuroinflammation and Behavioral Deficits in a Mouse Model of Sepsis-Associated Encephalopathy.Neuromolecular medicine · 2023Article
- Neurochemical effects of sepsis on the brain.Clinical science (London, England : 1979) · 2023Article
- Munc18-1 Contributes to Hippocampal Injury in Septic Rats Through Regulation of Syntanxin1A and Synaptophysin and Glutamate Levels.Neurochemical research · 2023Article
- Altered EEG, disrupted hippocampal long-term potentiation and neurobehavioral deficits implicate a delirium-like state in a mouse model of sepsis.Brain, behavior, and immunity · 2023Article
- P2X7 receptor contributes to long-term neuroinflammation and cognitive impairment in sepsis-surviving mice.Frontiers in pharmacology · 2023Article
- Article
- Brain innate immune response via miRNA-TLR7 sensing in polymicrobial sepsis.Brain, behavior, and immunity · 2022Article
- Central role of microglia in sepsis-associated encephalopathy: From mechanism to therapy.Frontiers in immunology · 2022Review
- The biological alterations of synapse/synapse formation in sepsis-associated encephalopathy.Frontiers in synaptic neuroscience · 2022Review
- Rapidly progressive brain atrophy in septic ICU patients: a retrospective descriptive study using semiautomatic CT volumetry.Critical care (London, England) · 2021Article
- Basic research and clinical progress of sepsis-associated encephalopathy.Journal of intensive medicine · 2021Review
- Manganese-induced reactive oxygen species activate IκB kinase to upregulate YY1 and impair glutamate transporter EAAT2 function in human astrocytes in vitro.Neurotoxicology · 2021Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Survivors from sepsis present long-term cognitive deficits and some of these alterations resemble the pathophysiological mechanisms of neurodegenerative diseases. For this reason, we analyzed beta-amyloid peptide (Aβ) and synaptophysin levels in the brain of rats that survived from sepsis and their relation to cognitive dysfunction and to acute brain inflammation. Sepsis was induced in rats by cecal ligation and puncture, and 30 days after surgery, the hippocampus and prefrontal cortex were isolated just after cognitive evaluation by the inhibitory avoidance test. The immunocontent of Aβ and synaptophysin were analyzed by Western blot analysis. Aβ increased and synaptophysin decreased in septic animals both in the hippocampus and prefrontal cortex concurrent with the presence of cognitive deficits. Prefrontal levels of synaptophysin correlated to the performance in the inhibitory avoidance. Two different treatments known to decrease brain inflammation and oxidative stress when administered at the acute phase of sepsis decreased Aβ levels both in the prefrontal cortex and hippocampus, increased synaptophysin levels only in the prefrontal cortex, and improved cognitive deficit in sepsis-survivor animals. In conclusion, we demonstrated that brain from sepsis-survivor animals presented an increase in Aβ content and a decrease in synaptophysin levels and cognitive impairment. These alterations can be prevented by treatments aimed to decrease acute brain inflammation and oxidative stress.
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