News Releases & Research Results Identification of genetic mutations of kinesin molecular motor KIF3B in schizophrenia

The research results led by Specially Appointed Professor Nobutaka Hirokawa, Specially Appointed Researcher Ashwaq Hassan Alsabban (at the time of the study), Specially Appointed Researcher Momo Morikawa, Lecturer Yosuke Tanaka, and Associate Professor Yosuke Takei (at the time of the study and currently professor at the University of Tsukuba) of the Department of Cell Biology and Anatomy, Graduate School of Medicine, University of Tokyo.

• Genetic mutations involved in the functional defects of the kinesin molecular motor “KIF3B” (*), which transports substances in cells, were identified by genetic exploration in schizophrenic patients.
  (*) A kinesin superfamily protein highly expressed in the nervous system.
• In a mouse experiment, mice lacking the KIF3B gene had the phenotype of schizophrenia, such as impaired sociality and an abnormal startle response, and hippocampal neurons showed significant abnormalities in synaptic morphology and functions.
• These are explained by the fact that the NR2A subunit of the NMDA glutamate receptor (NMDAR), which plays an important role in synaptic transmission, was transported by KIF3B.
• The results may provide a basis for developing treatments for schizophrenia associated with NMDAR.

This research was conducted with the support of Strategic Research Program for Brain Sciences of AMED.

The results were published in The EMBO Journal on November 20.

Ashwaq Hassan Alsabban, et al. Kinesin Kif3b mutation reduces NMDAR subunit NR2A trafficking and causes schizophrenia-like phenotypes in mice The EMBO Journal
DOI: 10.15252/embj.2018101090