Understanding the relationship between GSK-3 and Alzheimer’s disease: a focus on how GSK-3 can modulate synaptic plasticity processes

Abstract

Originally discovered because of its role in the regulation of glucose metabolism, GSK-3 is now widely recognized as a crucial player in many cellular functions. Control of GSK-3 activity occurs by complex mechanisms that are each dependent upon specific signaling pathways. Furthermore, GSK-3 dysfunction has been linked to a number of pathologies, including Alzheimer’s disease (AD). In particular, the involvement of GSK-3 in several key pathophysiological pathways leading to AD and neurodegenerative diseases has placed this enzyme in a central position in this disorder. In this article, the authors will specifically focus on the role of this enzyme as a key regulator of synaptic plasticity and how alterations in the GSK-3 synaptic functions may be a major factor in AD and other neurodegenerative disorders.

Keywords::

• Alzheimer’s
• dementia
• GSK-3
• long-term depression
• long-term potentiation
• memory
• neurodegeneration
• synaptic plasticity

Financial & competing interests disclosure

The authors were supported by Spanish Plan Nacional, CIBERNED and Comunidad de Madrid. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.