Identification of schizophrenia subgroups caused by white matter and myelin disorders

2017 Fiscal Year Final Research Report

• Project Area: Glial assembly: a new regulatory machinery of brain function and disorders
• Project/Area Number: 25117010
• Research Category: Grant-in-Aid for Scientific Research on Innovative Areas (Research in a proposed research area)
• Allocation Type: Single-year Grants
• Review Section: Biological Sciences
• Research Institution: Nagoya University
• Principal Investigator: Ozaki Norio 名古屋大学, 医学系研究科, 教授 (40281480)
• Co-Investigator(Renkei-kenkyūsha): IRITANI Shuji 名古屋大学, 大学院医学系研究科, 寄付講座教授 (60191904) ; IIDAKA Tetsuya 名古屋大学, 脳とこころの研究センター, 教授 (70324366) ; Branko Aleksic 名古屋大学, 大学院医学系研究科, 特任准教授 (60547511) ; HIRAKAWA Akihiro 東京大学, 大学院医学系研究科, 特任准教授 (90609330) ; NODA Yukihiro 名城大学, 薬学部, 教授 (90397464)
• Project Period (FY): 2013-06-28 – 2018-03-31
• Keywords: ゲノム / 神経科学 / 脳・神経 / 脳神経疾患 / 生体生命情報学

Outline of Final Research Achievements

We performed genomic analysis of schizophrenia, autism spectrum disorders (ASD) and bipolar disorder, identified variants strongly contributing to onset in RTN4R and CX3CR1 genes, and clarified their biological significance. RTN4R p.R292H mutation caused attenuation of interacting with its partner molecule LINGO-1 from in vitro functional analysis and revealed that it affected the formation of growth cones in elongating neurons (Kimuta et al., Translational Psychiatry, 2017). In addition, we also clarified that CX3CR1 p.A55T mutation caused structural instability by attenuating interaction with lipid molecules, and inhibited PI3K/Akt/mTOR signaling pathway (Ishizuka et al., Translational Psychiatry, 2017).

Free Research Field

医歯薬学