Involvement of the Glycogen Synthase Kinase-3 Signaling Pathway in TBI Pathology and Neurocognitive Outcome
2011

Glycogen Synthase Kinase-3 and Traumatic Brain Injury

Sample size: 10 publication 10 minutes Evidence: moderate

Author Information

Author(s): Dash Pramod K., Johnson Daniel, Clark Jordan, Orsi Sara A., Zhang Min, Zhao Jing, Grill Raymond J., Moore Anthony N., Pati Shibani

Primary Institution: The University of Texas Health Science Center at Houston

Hypothesis

Augmentation of GSK-3 inhibition post TBI would attenuate cell death and improve neurocognitive outcome in brain injured animals.

Conclusion

Selective inhibition of GSK-3 may offer partial cognitive improvement, with lithium providing neuroprotection and robust cognitive improvement.

Supporting Evidence

  • Post-injury administration of lithium significantly improved learning and memory in the Morris water maze task.
  • Lithium treatment preserved CA3 hippocampal neurons after TBI.
  • SB-216763 improved motor function but did not provide neuroprotection.

Takeaway

This study found that a drug called lithium can help protect the brain and improve memory after a brain injury.

Methodology

Using a rodent model, the study assessed the effects of lithium and a GSK-3 inhibitor on cognitive and motor functions after traumatic brain injury.

Potential Biases

Potential bias in behavioral assessments due to experimenter knowledge of treatment groups.

Limitations

The study primarily used a rodent model, which may not fully replicate human TBI outcomes.

Participant Demographics

Male Sprague-Dawley rats, 275–300 g.

Statistical Information

P-Value

p<0.05

Statistical Significance

p<0.05

Digital Object Identifier (DOI)

10.1371/journal.pone.0024648

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