ArticleAnesthesiology2020
Tau Contributes to Sevoflurane-induced Neurocognitive Impairment in Neonatal Mice.
Article in Anesthesiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 117 citations in OpenAlex.
- The NLRP3 Inflammasome: A Central Mediator in Sevoflurane-Induced Neurotoxicity and A Potential Target for Neuroprotection.Molecular neurobiology · 2026Review
- Estrogen Alleviates Sevoflurane-Induced Neurotoxicity by Inhibiting ERα-Tau Binding.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Omega-3 Polyunsaturated Fatty Acids Prevent Sevoflurane-induced Cognitive and Fine Motor Dysfunctions in Neonatal Mice by Enhancing Phosphorylated Tau Glymphatic System Clearance Pathway.Molecular neurobiology · 2025Article
- Identification of hub genes and pathways associated with sevoflurane-induced synaptic loss in diabetic offspring via comprehensive transcriptome analysis.Metabolic brain disease · 2025Article
- Estrogen improves sevoflurane-induced cognitive dysfunction by regulating synaptic zinc homeostasis.Molecular medicine (Cambridge, Mass.) · 2025Article
- Article
- Repeated Exposure to Sevoflurane in Neonatal Mice Induces Cognitive and Synaptic Impairments in a TTLL6-Mediated Tubulin Polyglutamylation Manner.CNS neuroscience & therapeutics · 2025Article
- Repeated sevoflurane exposure causes hypomyelination in the prefrontal cortex of adult male mice.Scientific reports · 2025Article
- Sevoflurane Suppresses Cardiomyocyte Pyroptosis in Myocardial Ischemia via NLRP3 Inflammasome Signaling.Analytical cellular pathology (Amsterdam) · 2025Article
- Review
- Dysregulation of the Gut Microbiota Contributes to Sevoflurane-Induced Cognitive Dysfunction in Aged Mice by Activating the NLRP3 Inflammasome.Molecular neurobiology · 2024Article
- Unraveling the role and mechanism of mitochondria in postoperative cognitive dysfunction: a narrative review.Journal of neuroinflammation · 2024Review
- Article
- Role of Tau Protein in Neurodegenerative Diseases and Development of Its Targeted Drugs: A Literature Review.Molecules (Basel, Switzerland) · 2024Review
- SHARPIN contributes to sevoflurane-induced neonatal neurotoxicity through up-regulating HMGB1 to repress M2 like-macrophage polarization.Metabolic brain disease · 2024Article
- MANF Alleviates Sevoflurane-Induced Cognitive Impairment in Neonatal Mice by Modulating Microglial Activation and Polarization.Molecular neurobiology · 2024Article
- Integrated ribosome and proteome analyses reveal insights into sevoflurane-induced long-term social behavior and cognitive dysfunctions through ADNP inhibition in neonatal mice.Zoological research · 2024Article
- Effect of General Anesthetic Agents on Microglia.Aging and disease · 2024Review
- HSP90 Inhibition Attenuated Isoflurane-Induced Neurotoxicity in Mice and Human Neuroglioma Cells.Neurochemical research · 2024Article
- Anesthesia-induced hippocampal-cortical hyperactivity and tau hyperphosphorylation impair remote memory retrieval in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
1 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors at 6 institutions in 2 countries.
Funding
Abstract
backgroundSevoflurane anesthesia induces Tau phosphorylation and cognitive impairment in neonatal but not in adult mice. This study tested the hypothesis that differences in brain Tau amounts and in the activity of mitochondria-adenosine triphosphate (ATP)-Nuak1-Tau cascade between the neonatal and adult mice contribute to the age-dependent effects of sevoflurane on cognitive function.
methods6- and 60-day-old mice of both sexes received anesthesia with 3% sevoflurane for 2 h daily for 3 days. Biochemical methods were used to measure amounts of Tau, phosphorylated Tau, Nuak1, ATP concentrations, and mitochondrial metabolism in the cerebral cortex and hippocampus. The Morris water maze test was used to evaluate cognitive function in the neonatal and adult mice.
resultsUnder baseline conditions and compared with 60-day-old mice, 6-day-old mice had higher amounts of Tau (2.6 ± 0.4 [arbitrary units, mean ± SD] vs. 1.3 ± 0.2; P < 0.001), Tau oligomer (0.3 ± 0.1 vs. 0.1 ± 0.1; P = 0.008), and Nuak1 (0.9 ± 0.3 vs. 0.3 ± 0.1; P = 0.025) but lesser amounts of ATP (0.8 ± 0.1 vs. 1.5 ± 0.1; P < 0.001) and mitochondrial metabolism (74.8 ± 14.1 [pmol/min] vs. 169.6 ± 15.3; P < 0.001) in the cerebral cortex. Compared with baseline conditions, sevoflurane anesthesia induced Tau phosphorylation at its serine 202/threonine 205 residues (1.1 ± 0.4 vs. 0.2 ± 0.1; P < 0.001) in the 6-day-old mice but not in the 60-day-old mice (0.05 ± 0.04 vs. 0.03 ± 0.01; P = 0.186). The sevoflurane-induced Tau phosphorylation and cognitive impairment in the neonatal mice were both attenuated by the inhibition of Nuak1 and the treatment of vitamin K2.
conclusionsHigher brain Tau concentrations and lower brain mitochondrial metabolism in neonatal compared with adult mice contribute to developmental stage-dependent cognitive dysfunction after sevoflurane anesthesia.
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