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Int. J. Mol. Sci. 2017, 18(10), 2044;

Dysbindin-1 Involvement in the Etiology of Schizophrenia

Department of Neuropharmacology and Drug Discovery, School of Pharmaceutical Sciences, Southern Medical University, Guangzhou 510515, China
School of Pharmacy Institute for Drug Research, Faculty of Medicine, The Hebrew University of Jerusalem, Jerusalem 91120, Israel
Faculty of Health Sciences, University of Macau, Taipa, Macau 999078, China
Zhuhai UM Science & Technology Research Institute, Zhuhai 519080, China
Author to whom correspondence should be addressed.
Received: 28 August 2017 / Revised: 16 September 2017 / Accepted: 19 September 2017 / Published: 22 September 2017
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Schizophrenia is a major psychiatric disorder that afflicts about 1% of the world’s population, falling into the top 10 medical disorders causing disability. Existing therapeutic strategies have had limited success on cognitive impairment and long-term disability and are burdened by side effects. Although new antipsychotic medications have been launched in the past decades, there has been a general lack of significant innovation. This lack of significant progress in the pharmacotherapy of schizophrenia is a reflection of the complexity and heterogeneity of the disease. To date, many susceptibility genes have been identified to be associated with schizophrenia. DTNBP1 gene, which encodes dysbindin-1, has been linked to schizophrenia in multiple populations. Studies on genetic variations show that DTNBP1 modulate prefrontal brain functions and psychiatric phenotypes. Dysbindin-1 is enriched in the dorsolateral prefrontal cortex and hippocampus, while postmortem brain studies of individuals with schizophrenia show decreased levels of dysbindin-1 mRNA and protein in these brain regions. These studies proposed a strong connection between dysbindin-1 function and the pathogenesis of disease. Dysbindin-1 protein was localized at both pre- and post-synaptic sites, where it regulates neurotransmitter release and receptors signaling. Moreover, dysbindin-1 has also been found to be involved in neuronal development. Reduced expression levels of dysbindin-1 mRNA and protein appear to be common in dysfunctional brain areas of schizophrenic patients. The present review addresses our current knowledge of dysbindin-1 with emphasis on its potential role in the schizophrenia pathology. We propose that dysbindin-1 and its signaling pathways may constitute potential therapeutic targets in the therapy of schizophrenia. View Full-Text
Keywords: schizophrenia; dysbindin-1; susceptibility gene; neurotransmitter release; neurite outgrowth schizophrenia; dysbindin-1; susceptibility gene; neurotransmitter release; neurite outgrowth

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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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Wang, H.; Xu, J.; Lazarovici, P.; Zheng, W. Dysbindin-1 Involvement in the Etiology of Schizophrenia. Int. J. Mol. Sci. 2017, 18, 2044.

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