GSK-3[beta] at the Intersection of Neuronal Plasticity and Neurodegeneration

In neurons, Glycogen Synthase Kinase-3[beta] (GSK-3j3) has been shown to regulate various critical processes underlying structural and functional synaptic plasticity. Mouse models with neuron-selective expression or deletion of GSK-3[beta] present behavioral and cognitive abnormalities, positioning...

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Bibliographic Details
Published inJournal of neural transplantation & plasticity Vol. 2019
Main Authors Jaworski, Tomasz, Banach-Kasper, Ewa, Gralec, Katarzyna
Format Journal Article
LanguageEnglish
Published John Wiley & Sons, Inc 31.05.2019
Subjects
Glycogen
Health aspects
Nervous system diseases
Neurons
Neurophysiology
Physiological aspects
Protein kinases
Synthesis
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Summary:In neurons, Glycogen Synthase Kinase-3[beta] (GSK-3j3) has been shown to regulate various critical processes underlying structural and functional synaptic plasticity. Mouse models with neuron-selective expression or deletion of GSK-3[beta] present behavioral and cognitive abnormalities, positioning this protein kinase as a key signaling molecule in normal brain functioning. Furthermore, mouse models with defective GSK-3[beta] activity display distinct structural and behavioral abnormalities, which model some aspects of different neurological and neuropsychiatric disorders. Equalizing GSK-3[beta] activity in these mouse models by genetic or pharmacological interventions is able to rescue some of these abnormalities. Thus, GSK-3[beta] is a relevant therapeutic target for the treatment of many brain disorders. Here, we provide an overview of how GSK-3[beta] is regulated in physiological synaptic plasticity and how aberrant GSK-3[beta] activity contributes to the development of dysfunctional synaptic plasticity in neuropsychiatric and neurodegenerative disorders.
ISSN:0792-8483
DOI:10.1155/2019/4209475