Sodium selenate retards epileptogenesis in acquired epilepsy models reversing changes in protein phosphatase 2A and hyperphosphorylated tau.
Abstract
There are no treatments in clinical practice known to mitigate the neurobiological processes that convert a healthy brain into an epileptic one, a phenomenon known as epileptogenesis. Downregulation of protein phosphatase 2A, a protein that causes the hyperphosphorylation of tau, is implicated in neurodegenerative diseases commonly associated with epilepsy, such as Alzheimer's disease and traumatic brain injury. Here we used the protein phosphatase 2A activator sodium selenate to investigate the role of protein phosphatase 2A in three different rat models of epileptogenesis: amygdala kindling, post-kainic acid status epilepticus, and post-traumatic epilepsy. Protein phosphatase 2A activity was decreased, and tau phosphorylation increased, in epileptogenic brain regions in all three models. Continuous sodium selenate treatment mitigated epileptogenesis and prevented the biochemical abnormalities, effects which persisted after drug withdrawal. Our studies indicate that limbic epileptogenesis is associated with downregulation of protein phosphatase 2A and the hyperphosphorylation of tau, and that targeting this mechanism with sodium selenate is a potential anti-epileptogenic therapy.
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In animal models of temporal lobe epilepsy, tau hyperphosphorylation is observed in the amygdala, hippocampus, and cortex following chemical and electrical amygdala kindling.
“In animal models of TLE, tau hyperphosphorylation is observed in relevant brain regions, including the amygdala, hippocampus, and cortex, following chemical and electrical amygdala kindling (Jones et al., 2012; Liu et al., 2016; Alves et al., 2019).”
From Tauopathy and Epilepsy Comorbidities and Underlying Mechanisms (2022) · cites this paper as Liu et al., 2016
The antiepileptic effects of sodium selenate persist following drug washout in animal traumatic brain injury models.
“The antiepileptic effects of sodium selenate persist following drug washout in animal TBI models (Liu et al., 2016), highlighting a potential disease-modifying effect of PP2A upregulation by sodium selenate during epileptogenesis when applied in early PTE disease stage.”
From Tauopathy and Epilepsy Comorbidities and Underlying Mechanisms (2022) · cites this paper as Liu et al., 2016
Long-lasting phosphatase downregulation occurs, as evidenced by decreased PP2A activity paired with increased p-tau levels in epileptogenic brain regions following post-kainic acid status epilepticus, amygdala kindling, and fluid percussion injury in rats.
“However, long-lasting phosphatase downregulation ultimately occurs, as evidenced by decreased PP2A activity paired with increased p-tau levels observed in epileptogenic brain regions following post-kainic acid status epilepticus, amygdala kindling, and fluid percussion injury in rats (Liu et al., 2016).”
From Tauopathy and Epilepsy Comorbidities and Underlying Mechanisms (2022) · cites this paper as Liu et al., 2016
Sodium selenate is a specific agonist for PP2A expressing the regulatory B subunit, an essential subunit for tau dephosphorylation by PP2A.
“Sodium selenate is a specific agonist for PP2A expressing the regulatory B subunit, an essential subunit for tau dephosphorylation by PP2A (Jones et al., 2012; Liu et al., 2016), and shows promise as a potential antiepileptic treatment option.”
From Tauopathy and Epilepsy Comorbidities and Underlying Mechanisms (2022) · cites this paper as Liu et al., 2016
Sodium selenate treatment attenuates seizure activity and tau hyperphosphorylation and accumulation following pentylenetetrazol or kainic acid administration and in the temporal lobe epilepsy model of amygdala kindling and the fluid percussion injury model of post-traumatic epilepsy.
“Sodium selenate treatment attenuates seizure activity and tau hyperphosphorylation and accumulation following administration of pentylenetetrazol or kainic acid as well as in the TLE model of amygdala kindling and the fluid percussion injury model of PTE (Jones et al., 2012; Liu et al., 2016).”
From Tauopathy and Epilepsy Comorbidities and Underlying Mechanisms (2022) · cites this paper as Liu et al., 2016
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Mechanistic and therapeutic relationships of traumatic brain injury and γ-amino-butyric acid (GABA)
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Astrocytic IGF‐1 and IGF‐1R Orchestrate Mitophagy in Traumatic Brain Injury via Exosomal miR‐let‐7e
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Self-citationInhibition of Death-associated Protein Kinase 1 protects against Epileptic Seizures in mice
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Knowledge atlas of post-traumatic epilepsy research: Based on citespace visualization analysis
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Self-citationThe role of Rho/ROCK in epileptic seizure-related neuronal damage
Wang, Z., Ren, D., & Zheng, P. (2022) · Metabolic Brain Disease · doi:10.1007/s11011-022-00909-6 · Cited by 15 · see citing works
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Effects of altered tau expression on dentate granule cell excitability in mice
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Antiepileptic Drugs as Potential Dementia Prophylactics Following Traumatic Brain Injury
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Early life adversity accelerates epileptogenesis and enhances depression-like behaviors in rats
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Self-citationAssociations between Serum Tau, Neurological Outcome, and Cognition following Traumatic Brain Injury
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Self-citationPost-Traumatic Epilepsy in Zebrafish Is Drug-Resistant and Impairs Cognitive Function
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Vivash, L. E., Johns, H. T., Churilov, L. P., MacPhail, S., Casillas-Espinosa, P. M., Malpas, C. B., Shultz, S. R., Tailby, C., Wijayath, M., Reutens, D. C., et al. (2023) · BMJ Open · doi:10.1136/bmjopen-2023-075888 · Cited by 9 · see citing works
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Self-citationDisease-Modifying Effects of Neural Regeneration Peptide 2945 in the GAERS Model of Absence Epilepsy
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Research Progress on the Immune-Inflammatory Mechanisms of Posttraumatic Epilepsy
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- Authors
- Liu, S.-J., Zheng, P., Wright, D. K., Dezsi, G., Braine, E., Nguyen, T., Corcoran, N. M., Johnston, L. A., Hovens, C. M., Mayo, J. N., Hudson, M., Shultz, S. R., Jones, N. C., & O’Brien, T. J.
- Affiliations
- The Royal Melbourne Hospital (AU)
- The University of Melbourne (AU)
- ORCID
- Venue
- Brain
- Publisher
- Oxford University Press (OUP)
- Published
- 2016-06-11
- Volume
- 139
- Issue
- 7
- Pages
- 1919-1938
- ISSN
- 0006-8950 (ISSN-L)
- 1460-2156
- OpenAlex
- W2412978786
- Cited by
- 127
- References
- 57
- Citations by year
- 2026: 6 · 2025: 10 · 2024: 13 · 2023: 14 · 2022: 12 · 2021: 18 · 2020: 11 · 2019: 20 · 2018: 11 · 2017: 11 · 2016: 1
- FWCI
- 12.74
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Brain (publishedVersion)
- PubMed (publishedVersion)
- HighWire Press Open Archive (submittedVersion)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Epilepsy research and treatment
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Pharmacological Effects and Toxicity Studies
- Keywords
- sodium selenate, epileptogenesis, protein phosphatase 2A, tau hyperphosphorylation, acquired epilepsy, amygdala kindling, status epilepticus, post-traumatic epilepsy, limbic epilepsy, drug withdrawal
- MeSH terms
- Brain Injuries, Traumatic, Animals, Anticonvulsants, Brain, Disease Models, Animal, Electroencephalography, Epilepsy, Kainic Acid, Kindling, Neurologic, Magnetic Resonance Imaging, Male, Phosphorylation, tau Proteins, Rats, Wistar, Excitatory Amino Acid Agonists, Rats, Protein Phosphatase 2, Selenic Acid
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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