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Use of a Wireless Video-EEG System to Monitor Epileptiform Discharges Following Lateral Fluid-Percussion Induced Traumatic Brain Injury
Published on: June 21, 2019
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Tau Phosphorylation Patterns in the Rat Cerebral Cortex After Traumatic Brain Injury and Sodium Selenate Effects: An
Patricia Grandizoli Saletti1, Pablo M Casillas-Espinosa2,3,4, Christos Panagiotis Lisgaras1
1Saul R. Korey Department of Neurology, Laboratory of Developmental Epilepsy, Albert Einstein College of Medicine, Bronx New York, USA.
Journal of Neurotrauma
|March 23, 2023
Summary
Sodium selenate (SS) shows potential in reducing phosphorylated tau (pTAU) after traumatic brain injury (TBI) in rats. Further research is needed to clarify SS effects on pTAU and protein phosphatase 2A (PP2A) in TBI models.
Area of Science:
- Neuroscience
- Biochemistry
- Pharmacology
Background:
- Traumatic brain injury (TBI) is associated with increased levels of phosphorylated tau (pTAU).
- Protein phosphatase 2A (PP2A) plays a role in dephosphorylating tau protein.
- Sodium selenate (SS) is known to activate PP2A.
Purpose of the Study:
- To investigate the efficacy of sodium selenate (SS) in a lateral fluid percussion injury (LFPI) model of TBI.
- To examine the effects of SS on pTAU levels and PP2A activity in the TBI model.
- To assess SS as a potential therapeutic agent for TBI.
Main Methods:
- Adult male rats were subjected to LFPI or sham procedures at two international sites.
- Rats received varying doses of SS or vehicle post-injury.
- Brain tissue was analyzed using immunohistochemistry (IHC), Western blots (WB), and PP2A activity assays.
- Motor function was assessed using neuroscores.
Main Results:
- LFPI induced time- and form-specific increases in cortical pTAU ipsilateral to the injury.
- PP2A activity was reduced in LFPI rats compared to sham controls.
- SS treatment reduced cortical pTAU levels (WB) and increased PP2A activity and PR55 expression (WB) in a dose-dependent manner.
- SS did not significantly alter neuroscores or cellular pTAU/PR55 levels in IHC.
Conclusions:
- The study confirms LFPI-induced increases in cortical pTAU and suggests a role for PP2A.
- SS demonstrates potential in reducing pTAU and enhancing PP2A activity in a TBI model.
- Further investigation is warranted to elucidate the mechanisms and optimize SS treatment for TBI.
