Schizophrenia is a common disease with a lifetime prevalence of about 1% worldwide, and it is a chronic mental disorder for which an understanding of the onset mechanism is desired. However, it is thought to be due to a disorder in the communication between neurons via neurotransmitters, but it has not been fully elucidated. α1,6-Fucosyltransferase (Fut8)-deficient mice show abnormalities in the formation of complexes of ion channel-type glutamate receptors (AMPA receptors) that play important roles in synaptic plasticity and synaptic transmission [1]. Interestingly, a decrease in Fut8 expression in the superior temporal gyrus, which is responsible for social cognition in part of the temporal lobe, has been reported in studies using postmortem brains of elderly schizophrenia patients. Also, a region-specific decrease in polysialic acid has been observed in patient brains. Furthermore, in DISC1 mutant mice, a risk gene for schizophrenia, the expression of polysialic acid in the suprachiasmatic nucleus decreases, and its length also shortens, suggesting that α2,8 sialic acid transferase ST8SIA2/STX plays an important role [2]. In recent years, neuroinflammation has been attracting attention as a cause of schizophrenia. In Fut8 homozygous knockout mice and heterozygous knockout mice, microglia, which are responsible for brain immunity, are easily activated [3]. Also, polysialic acid (polySia-NCAM) on the surface of microglial cells quickly disappears due to the action of sialidase when it receives inflammatory stimuli [4]. By clarifying how α1,6 fucose (also called core fucose) and polysialic acid act on the activity of microglia, glycan correction may become a new target for the prevention and treatment of schizophrenia.