Abstract
Schizophrenia is a disabling illness with limited treatment options. The underlying pathophysiology remains unknown, partially due to its heterogeneous nature, and a lack of understanding of the biological functions of genetic risk factors. Several signaling pathways have been implicated, however, with the varying degrees of support. In this article, I will focus on the converging evidence supporting a prominent role for Wnt and glycogen synthase kinase 3 (GSK3) signaling in the biological bases of schizophrenia. This includes current pharmacological therapies that target GSK3, animal model and cell-based studies, and recent human genetic findings that implicate Wnt and GSK3 signaling.
© 2013 John Wiley & Sons A/S. Published by Blackwell Publishing Ltd.
MeSH terms
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Animals
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Antipsychotic Agents / therapeutic use
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DNA Copy Number Variations
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Glycogen Synthase Kinase 3 / genetics*
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Glycogen Synthase Kinase 3 / metabolism
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Humans
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Models, Genetic
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Nerve Tissue Proteins / genetics
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Nerve Tissue Proteins / metabolism
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Proto-Oncogene Proteins c-akt / genetics
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Proto-Oncogene Proteins c-akt / metabolism
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Receptors, Dopamine / genetics
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Receptors, Dopamine / metabolism
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Schizophrenia / drug therapy
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Schizophrenia / genetics*
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Schizophrenia / physiopathology
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Signal Transduction / drug effects
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Signal Transduction / genetics*
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Signal Transduction / physiology
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Wnt Signaling Pathway / drug effects
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Wnt Signaling Pathway / genetics
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Wnt Signaling Pathway / physiology
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Wnt1 Protein / genetics*
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Wnt1 Protein / metabolism
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beta Catenin / genetics
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beta Catenin / metabolism
Substances
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Antipsychotic Agents
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DISC1 protein, human
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Nerve Tissue Proteins
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Receptors, Dopamine
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Wnt1 Protein
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beta Catenin
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Proto-Oncogene Proteins c-akt
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Glycogen Synthase Kinase 3