Schizophrenia (SCZ) is a serious mental illness that affects approximately 1% of the world’s population and causes a loss of integration between thoughts and emotions. Its symptoms cause significant impairment in daily life and have a major social impact, making the development of treatment methods an urgent issue. SCZ is currently believed to be caused by functional disorders in specific areas of the brain during its developmental stages, and initial imaging diagnostics have revealed a reduction in the volume of gray matter and the olfactory bulb. Regarding glycans, the involvement of polysialic acid (polySia, PSA) has been reported. Postmortem analysis of SCZ brains has reported a decrease in polySia-expressing cells in the prefrontal cortex and hippocampus. On the other hand, genome analysis has revealed numerous statistically significant single-nucleotide polymorphisms (SNPs) in the polysialyltransferase ST8SIA2, and some of these have been reported to result in reduced polySia production and impaired function through biochemical analysis [1, 2]. Also, ST8Sia2-deficient mice exhibit SCZ-like phenotypes [3]. Furthermore, an increase in polySia chains with schizophrenia treatment drugs has been reported using human neural cells and mouse individuals [1]. There are also reports that the blood dynamics of polySia chains are involved in the disease [4, 5]. Therefore, the mechanism of expression control of polySia chains may be involved in the disease, and there is a possibility of developing new diagnostic drugs and therapeutic drugs.