Lithium inhibits GSK-3 through disruption of Striatal β-Arrestin, PP2A, and Akt Signaling

Authors

  • GO Oladipo Applied Clinical and Computational Biochemistry Unit, Department of Biochemistry, Achievers University, Owo, Nigeria
  • MC Oladipo Microbial Enzyme Biotechnology and Bioremediation Unit, Department of Biochemistry, Achievers University, Owo, Nigeria
  • T Olusanya Biomaterials & Drug Delivery Research Group, University of Portsmouth, United Kingdom.
  • OE Ibukun Applied Clinical Biochemistry Research Unit, Department of Biochemistry, Federal University of Technology, Akure, Nigeria.
  • OA Akinola Applied Clinical Biochemistry Research Unit, Department of Biochemistry, Federal University of Technology, Akure, Nigeria.

Keywords:

β-Arrestin, Lithium, GSK-3, PP2A, Neuroprotection

Abstract

β-Arrestin, PP2A, and Akt form a signaling complex that affects the activation of GSK-3. GSK-3 affects the pathway leading to neurodegenerative diseases. Lithium is a known mood stabilizer which exhibits a direct or indirect inhibition of GSK-3. GSK-3 is the link between neurodegeneration and the mitigating potential of lithium via the direct and indirect inhibition of this enzyme. This review reveals the mechanisms associated with lithium neuroprotection and the synergies between β-arrestin, PP2A, AKT, and GSK-3, the limiting effects on the progression of neurodegeneration.

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Published

2023-12-25

Issue

Vol. 5 No. 2 (2023): Special Issue for AUCONAS Conference 2023

Section

Review Articles