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Sodium selenate retards epileptogenesis in acquired epilepsy models reversing changes in protein phosphatase 2A and

Shi-Jie Liu1, Ping Zheng1, David K Wright2

  • 11 Department of Medicine, Melbourne Brain Centre, The Royal Melbourne Hospital, The University of Melbourne, Parkville, VIC, Australia.

Brain : a Journal of Neurology
|June 13, 2016
PubMed

Insights

This study reveals that targeting protein phosphatase 2A (PP2A) with sodium selenate may prevent epilepsy development. This approach shows promise for treating neurodegenerative diseases and preventing epileptogenesis.

Area of Science:

  • Neuroscience
  • Biochemistry
  • Epilepsy Research

Background:

  • Epileptogenesis, the process of developing epilepsy, lacks clinical treatments targeting its underlying neurobiology.
  • Downregulation of protein phosphatase 2A (PP2A) and subsequent tau hyperphosphorylation are linked to epilepsy comorbidities like Alzheimer's disease and traumatic brain injury.

Purpose of the Study:

  • To investigate the role of PP2A in three distinct rat models of epileptogenesis.
  • To evaluate the anti-epileptogenic potential of sodium selenate, a PP2A activator.

Main Methods:

  • Utilized three rat models: amygdala kindling, post-kainic acid status epilepticus, and post-traumatic epilepsy.
  • Administered sodium selenate to assess its effects on epileptogenesis and biochemical markers.
  • Measured PP2A activity and tau phosphorylation levels in affected brain regions.

Main Results:

  • All three models showed decreased PP2A activity and increased tau phosphorylation in epileptogenic brain areas.
  • Continuous sodium selenate treatment effectively mitigated epileptogenesis and reversed biochemical abnormalities.
  • These beneficial effects persisted even after the cessation of sodium selenate treatment.

Conclusions:

  • Limbic epileptogenesis is associated with reduced PP2A activity and elevated tau phosphorylation.
  • Sodium selenate demonstrates potential as an anti-epileptogenic therapy by targeting the PP2A-tau pathway.
Keywords:
MRIPR55animal modelepilepsytraumatic brain injury

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