2017 Fiscal Year Final Research Report
Involvement of Cxcl12/Cxcr4 signaling deficits in schizophrenia
Project/Area Number |
26293074
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Research Category |
Grant-in-Aid for Scientific Research (B)
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Allocation Type | Partial Multi-year Fund |
Section | 一般 |
Research Field |
Pathological medical chemistry
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Research Institution | Research Institute, Shiga Medical Center |
Principal Investigator |
Tanigaki Kenji 滋賀県立成人病センター(研究所), 神経病態研究部門, 専門研究員 (70362473)
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Project Period (FY) |
2014-04-01 – 2018-03-31
|
Keywords | 統合失調症 / Cxcr4 / Cxcl12 / ケモカイン |
Outline of Final Research Achievements |
22q11 deletion syndrome is a chromosome disorder. 20-30% of the patients with this deletion develop schizophrenia. We previously showed that the heterozygous deletion of Dgcr8 caused Cxcl12/Cxcr4 signaling deficits, leading to developmental abnormalities in the dentate gyrus of the hippocampus and interneruons. In this study, we examined whether Cxcl12/Cxcr4 signal deficits can cause schizophrenia-like behavioral abnormalities using Cxcr4-floxed mice, and whether Cxcl12/Cxcr4 signal deficits exist in sporadic schizophrenia patients using lymphodblastic cell lines.
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Free Research Field |
神経科学、精神医学
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