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Multiple Sclerosis and Schizophrenia
Review

Dysbindin-1 Involvement in the Etiology of Schizophrenia

1
Department of Neuropharmacology and Drug Discovery, School of Pharmaceutical Sciences, Southern Medical University, Guangzhou 510515, China
2
School of Pharmacy Institute for Drug Research, Faculty of Medicine, The Hebrew University of Jerusalem, Jerusalem 91120, Israel
3
Faculty of Health Sciences, University of Macau, Taipa, Macau 999078, China
4
Zhuhai UM Science & Technology Research Institute, Zhuhai 519080, China
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2017, 18(10), 2044; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms18102044
Received: 28 August 2017 / Revised: 16 September 2017 / Accepted: 19 September 2017 / Published: 22 September 2017
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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MDPI and ACS Style

Wang, H.; Xu, J.; Lazarovici, P.; Zheng, W. Dysbindin-1 Involvement in the Etiology of Schizophrenia. Int. J. Mol. Sci. 2017, 18, 2044. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms18102044

AMA Style

Wang H, Xu J, Lazarovici P, Zheng W. Dysbindin-1 Involvement in the Etiology of Schizophrenia. International Journal of Molecular Sciences. 2017; 18(10):2044. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms18102044

Chicago/Turabian Style

Wang, Haitao, Jiangping Xu, Philip Lazarovici, and Wenhua Zheng. 2017. "Dysbindin-1 Involvement in the Etiology of Schizophrenia" International Journal of Molecular Sciences 18, no. 10: 2044. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms18102044

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