Open Access

Association of glycogen synthase kinase‑3β with Parkinson's disease (Review)

  • Authors:
    • Da‑Wei Li
    • Zhi‑Qiang Liu
    • Wei Chen
    • Min Yao
    • Guang‑Ren Li
  • View Affiliations

  • Published online on: March 28, 2014     https://doi.org/10.3892/mmr.2014.2080
  • Pages: 2043-2050
  • Copyright: © Li et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY_NC 3.0].

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Glycogen synthase kinase‑3 (GSK‑3) is a pleiotropic serine/threonine protein kinase found in almost all eukaryotes. It is structurally highly conserved and has been identified as a multifaceted enzyme affecting a wide range of biological functions, including gene expression and cellular processes. There are two closely related isoforms of GSK‑3; GSK‑3α and GSK‑3β. The latter appears to play crucial roles in regulating the pathogenesis of diverse diseases, including neurodegenerative disease. The present review focuses on the involvement of this protein in Parkinson's disease (PD), a common neurodegenerative disorder characterized by the gradually progressive and selective loss of dopaminergic neurons, and by intracellular inclusions known as Lewy bodies (LBs) expressed in surviving neurons of the substantia nigra (SN). GSK‑3β is involved in multiple signaling pathways and has several phosphorylation targets. Numerous apoptotic conditions can be facilitated by the GSK‑3β signaling pathways. Studies have shown that GSK‑3β inhibition protects the dopaminergic neurons from various stress‑induced injuries, indicating the involvement of GSK‑3β in PD pathogenesis. However, the underlying mechanisms of the protective effect of GSK‑3β inhibition on dopaminergic neurons in PD is not completely understood. Multiple pathological events have been recognized to be responsible for the loss of dopaminergic neurons in PD, including mitochondrial dysfunction, oxidative stress, protein aggregation and neuroinflammation. The present review stresses the regulatory roles of GSK‑3β in these events and in dopaminergic neuron degeneration, in an attempt to gain an improved understanding of the underlying mechanisms and to provide a potential effective therapeutic target for PD.
View Figures
View References

Related Articles

Journal Cover

June-2014
Volume 9 Issue 6

Print ISSN: 1791-2997
Online ISSN:1791-3004

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Li DW, Liu ZQ, Chen W, Yao M and Li GR: Association of glycogen synthase kinase‑3β with Parkinson's disease (Review). Mol Med Rep 9: 2043-2050, 2014.
APA
Li, D., Liu, Z., Chen, W., Yao, M., & Li, G. (2014). Association of glycogen synthase kinase‑3β with Parkinson's disease (Review). Molecular Medicine Reports, 9, 2043-2050. https://doi.org/10.3892/mmr.2014.2080
MLA
Li, D., Liu, Z., Chen, W., Yao, M., Li, G."Association of glycogen synthase kinase‑3β with Parkinson's disease (Review)". Molecular Medicine Reports 9.6 (2014): 2043-2050.
Chicago
Li, D., Liu, Z., Chen, W., Yao, M., Li, G."Association of glycogen synthase kinase‑3β with Parkinson's disease (Review)". Molecular Medicine Reports 9, no. 6 (2014): 2043-2050. https://doi.org/10.3892/mmr.2014.2080