GSK-3β at the Intersection of Neuronal Plasticity and Neurodegeneration

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

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Main Authors: Tomasz Jaworski, Ewa Banach-Kasper, Katarzyna Gralec
Format: Article
Language:English
Published: Wiley 2019-01-01
Series:Neural Plasticity
Online Access:http://dx.doi.org/10.1155/2019/4209475
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author Tomasz Jaworski
Ewa Banach-Kasper
Katarzyna Gralec
author_facet Tomasz Jaworski
Ewa Banach-Kasper
Katarzyna Gralec
author_sort Tomasz Jaworski
collection DOAJ
description In neurons, Glycogen Synthase Kinase-3β (GSK-3β) has been shown to regulate various critical processes underlying structural and functional synaptic plasticity. Mouse models with neuron-selective expression or deletion of GSK-3β present behavioral and cognitive abnormalities, positioning this protein kinase as a key signaling molecule in normal brain functioning. Furthermore, mouse models with defective GSK-3β activity display distinct structural and behavioral abnormalities, which model some aspects of different neurological and neuropsychiatric disorders. Equalizing GSK-3β activity in these mouse models by genetic or pharmacological interventions is able to rescue some of these abnormalities. Thus, GSK-3β is a relevant therapeutic target for the treatment of many brain disorders. Here, we provide an overview of how GSK-3β is regulated in physiological synaptic plasticity and how aberrant GSK-3β activity contributes to the development of dysfunctional synaptic plasticity in neuropsychiatric and neurodegenerative disorders.
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spelling doaj-art-e59a7cdb7b164014bdd95086d728baf62025-02-03T06:01:10ZengWileyNeural Plasticity2090-59041687-54432019-01-01201910.1155/2019/42094754209475GSK-3β at the Intersection of Neuronal Plasticity and NeurodegenerationTomasz Jaworski0Ewa Banach-Kasper1Katarzyna Gralec2Laboratory of Animal Models, Nencki Institute of Experimental Biology PAS, 02-093 Warsaw, PolandLaboratory of Animal Models, Nencki Institute of Experimental Biology PAS, 02-093 Warsaw, PolandLaboratory of Animal Models, Nencki Institute of Experimental Biology PAS, 02-093 Warsaw, PolandIn neurons, Glycogen Synthase Kinase-3β (GSK-3β) has been shown to regulate various critical processes underlying structural and functional synaptic plasticity. Mouse models with neuron-selective expression or deletion of GSK-3β present behavioral and cognitive abnormalities, positioning this protein kinase as a key signaling molecule in normal brain functioning. Furthermore, mouse models with defective GSK-3β activity display distinct structural and behavioral abnormalities, which model some aspects of different neurological and neuropsychiatric disorders. Equalizing GSK-3β activity in these mouse models by genetic or pharmacological interventions is able to rescue some of these abnormalities. Thus, GSK-3β is a relevant therapeutic target for the treatment of many brain disorders. Here, we provide an overview of how GSK-3β is regulated in physiological synaptic plasticity and how aberrant GSK-3β activity contributes to the development of dysfunctional synaptic plasticity in neuropsychiatric and neurodegenerative disorders.http://dx.doi.org/10.1155/2019/4209475
spellingShingle Tomasz Jaworski
Ewa Banach-Kasper
Katarzyna Gralec
GSK-3β at the Intersection of Neuronal Plasticity and Neurodegeneration
Neural Plasticity
title GSK-3β at the Intersection of Neuronal Plasticity and Neurodegeneration
title_full GSK-3β at the Intersection of Neuronal Plasticity and Neurodegeneration
title_fullStr GSK-3β at the Intersection of Neuronal Plasticity and Neurodegeneration
title_full_unstemmed GSK-3β at the Intersection of Neuronal Plasticity and Neurodegeneration
title_short GSK-3β at the Intersection of Neuronal Plasticity and Neurodegeneration
title_sort gsk 3β at the intersection of neuronal plasticity and neurodegeneration
url http://dx.doi.org/10.1155/2019/4209475
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