ArticleNeurobiology of disease2015
Reactive oxygen species mediate cognitive deficits in experimental temporal lobe epilepsy.
Article in Neurobiology of disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.
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Who cites it
58 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Relationship between acute glucose variability and cognitive decline in type 2 diabetes: A systematic review and meta-analysis.PloS one · 2023Pooled it
- The Biomarkers and Underlying Mechanisms of Mitochondrial and Programmed Cell Death Related Genes in Epilepsy by Combining Transcriptome and Single-Cell Sequencing.Journal of Korean Neurosurgical Society · 2026Article
- Article
- Reactive Oxygen Species Regulation Across Retinitis Pigmentosa Animal Models: A 25-Year Systematized Review.Molecular neurobiology · 2025Review
- Manganese Superoxide Dismutase: Structure, Function, and Implications in Human Disease.Antioxidants (Basel, Switzerland) · 2025Review
- The Oxidative Stress in Epilepsy-Focus on Melatonin.International journal of molecular sciences · 2024Review
- Comparative Proteomic Profiling of Blood Plasma Revealed Marker Proteins Involved in Temporal Lobe Epilepsy.International journal of molecular sciences · 2024Article
- Superoxide dismutase and neurological disorders.IBRO neuroscience reports · 2024Review
- Influence of Long-Term Anti-Seizure Medications on Redox Parameters in Human Blood.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Novel Catalytic Antioxidant Formulation Decreases Oxidative Stress, Neuroinflammation and Cognitive Dysfunction in a Model of Nerve Agent Intoxication.The Journal of pharmacology and experimental therapeutics · 2024Article
- The microRNA-211-5p/P2RX7/ERK/GPX4 axis regulates epilepsy-associated neuronal ferroptosis and oxidative stress.Journal of neuroinflammation · 2024Article
- Unveiling the hidden connection: the blood-brain barrier's role in epilepsy.Frontiers in neurology · 2024Review
- Cognitive comorbidities in the rat pilocarpine model of epilepsy.Frontiers in neurology · 2024Article
- Repeated episodes of postictal hypoxia are a mechanism for interictal cognitive impairments.Scientific reports · 2023Article
- Pre- and Post-Endurance Training Mitigates the Rat Pilocarpine-Induced Status Epilepticus and Epileptogenesis-Associated Deleterious Consequences.International journal of molecular sciences · 2022Article
- Crosstalk between neuroinflammation and oxidative stress in epilepsy.Frontiers in cell and developmental biology · 2022Review
- Neuron-specific mitochondrial oxidative stress results in epilepsy, glucose dysregulation and a striking astrocyte response.Neurobiology of disease · 2021Article
- Mechanisms of disease-modifying effect of saracatinib (AZD0530), a Src/Fyn tyrosine kinase inhibitor, in the rat kainate model of temporal lobe epilepsy.Neurobiology of disease · 2021Article
- Effects of Lacosamide Treatment on Epileptogenesis, Neuronal Damage and Behavioral Comorbidities in a Rat Model of Temporal Lobe Epilepsy.International journal of molecular sciences · 2021Article
- Role of Modulation of Hippocampal Glucose Following Pilocarpine-Induced Status Epilepticus.Molecular neurobiology · 2021Article
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Authors and funding
6 authors.
Funding
Abstract
Cognitive dysfunction is an important comorbidity of temporal lobe epilepsy (TLE). However, no targeted therapies are available and the mechanisms underlying cognitive impairment, specifically deficits in learning and memory associated with TLE remain unknown. Oxidative stress is known to occur in the pathogenesis of TLE but its functional role remains to be determined. Here, we demonstrate that oxidative stress and resultant processes contribute to cognitive decline associated with epileptogenesis. Using a synthetic catalytic antioxidant, we show that pharmacological removal of reactive oxygen species (ROS) prevents 1) oxidative stress, 2) deficits in mitochondrial oxygen consumption rates, 3) hippocampal neuronal loss and 4) cognitive dysfunction without altering the intensity of the initial status epilepticus (SE) or epilepsy development in a rat model of SE-induced TLE. Moreover, the effects of the catalytic antioxidant on cognition persisted beyond the treatment period suggestive of disease-modification. The data implicate oxidative stress as a novel mechanism by which cognitive dysfunction can arise during epileptogenesis and suggest a potential disease-modifying therapeutic approach to target it.
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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.