Updated on 2025/07/10

写真a

 
OHGIDANI Masahiro
 
Organization
School of Medicine Medical Course Basic Medicine Anatomy[Functional Anatomy and Neuroscience]
External link

Research Interests

  • トランスレーショナル研究

  • 医用生体工学

  • 神経免疫

  • 生物学的精神医学

  • ミクログリア

  • 精神神経疾患

  • 解剖学

Research Areas

  • Life Science / Anatomy

  • Life Science / Psychiatry

Papers

  • Expression of Kallikrein in Glial Cells and Its Influence on Oligodendrocyte Myelination. Reviewed International journal

    Yusuke Tanaka, Eriko Furube, Shigetaka Yoshida, Masahiro Ohgidani

    Journal of neurochemistry   169 ( 7 )   e70150   2025.7

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    Authorship：Last author,　Corresponding author   Language：English   Publishing type：Research paper (scientific journal)  

    Appropriate myelin structures are crucial for efficient nerve impulse conduction; however, the precise mechanisms sustaining myelin integrity throughout life remain unclear. KLK6 and KLK8 (Klk8 in mice), serine proteases of the tissue kallikrein family, are upregulated in oligodendrocytes in response to central nervous system injuries and are associated with myelin degradation. However, the physiological roles of these proteases have not yet been fully clarified. Here, we examined whether Klk8 and Klk6 are expressed in glial cells other than oligodendrocytes and whether Klk8 affects myelin structure under physiological conditions. Microglia, oligodendrocytes, and astrocytes were isolated from the brains and spinal cords of wild-type and Klk8 knockout mice, and we examined the expression levels of Klk8, Klk6, and myelin-related genes. We found that both Klk6 and Klk8 expression levels in oligodendrocytes were correlated with myelin-related gene expression levels. The myelin-related gene expression levels in oligodendrocytes were significantly higher in Klk8 knockout mice than in wild-type mice. Immunohistochemistry, western blotting, and transmission electron microscopy revealed that, compared with that in wild-type mice, the myelin volume and thickness were greater in Klk8 knockout mice. Oligodendrocyte-expressed Klk8 may play a role in modulating myelin structure under physiological conditions. Klk8 expression was higher in microglia than in oligodendrocytes, and Klk6 expression was higher in astrocytes than in oligodendrocytes. The expression levels of Klk6 and Klk8 in microglia and astrocytes were uncorrelated with the expression of myelin-related genes in oligodendrocytes, suggesting that these genes in microglia and astrocytes may have functional roles other than myelination.

    DOI： 10.1111/jnc.70150

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  • The flow cytometric analysis of depression focusing on modern-type depression and hikikomori: Exploring the link between subtypes of depression and immunological imbalances. Reviewed International journal

    Keitaro Matsuo, Mitsuru Watanabe, Shogo Inamine, Toshio Matsushima, Sota Kyuragi, Yasuhiro Maeda, Ryoko Katsuki, Masahiro Ohgidani, Ryo Yamasaki, Noriko Isobe, Tomohiro Nakao, Takahiro A Kato

    Dialogues in clinical neuroscience   27 ( 1 )   13 - 25   2025.1

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    INTRODUCTION: Depression includes different phenotypes. Modern-type depression (MTD) is a gateway disorder to pathological social withdrawal, known as hikikomori. Adverse childhood experiences (ACEs) are also important aetiologies of depression. Recently, immune imbalance has been proposed as a biological basis of depression. We hypothesised that peripheral immunological characteristics may be involved in subtyping of depression. METHODS: 21 patients with major depressive disorder (MDD) and 24 healthy controls (HC) were recruited. Peripheral blood mononuclear cells (PBMCs) were examined for surface antigens by flow cytometry. Participants were administered psychological scales such as Patient Health Questionnaire (PHQ)-9, Modern-Type Depression Trait Scale (TACS-22), Hikikomori Questionnaire (HQ-25), Child Abuse and Trauma Scale (CATS). RESULTS: MDD group showed significantly higher percentage of B cells than HC group (p = 0.032). MDD group presented a negative correlation between: PHQ-9 and CD8 T effector memory cells (r= -0.639, p = 0.002), TACS-22 and monocytes (r= -0.459, p = 0.036), HQ-25 and NK T cells (r= -0.638, p = 0.004), CATS and Intermediate monocytes (r= -0.594, p = 0.009). CONCLUSIONS: MTD traits, hikikomori tendencies, and ACEs were correlated with specific characteristics of peripheral immune cells. Our results suggest that immune imbalance influences the diverse presentations of depression. Further validation is warranted by large-scale prospective studies.

    DOI： 10.1080/19585969.2025.2452842

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  • Human monocyte‐derived microglia‐like (<scp>iMG</scp>) cells: A tool to explore microglial dynamics Reviewed

    Sota Kyuragi, Shogo Inamine, Masahiro Ohgidani, Takahiro A. Kato

    Clinical and Experimental Neuroimmunology   2024.9

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    Publishing type：Research paper (scientific journal)   Publisher：Wiley  

    Abstract

    Recent studies have highlighted the importance of microglia as key immunomodulators in a variety of neuropsychiatric diseases. Postmortem brain analysis and positron emission tomography are representative research approaches to assess microglial activation in human patients and this research has revealed microglial activation in the brains of patients with various neuropsychiatric disorders. However, only limited aspects of microglial activation can be assessed with these methods. To overcome the technical and ethical limitations of collecting human‐derived microglia in brain biopsies, we first developed a method to generate directly induced microglia‐like (iMG) cells from fresh human peripheral blood monocytes in 2014. These iMG cells can be used to perform dynamic morphological and molecular analyses regarding phagocytic capacity and cytokine release following stress stimulation at the cellular level. Patient‐derived iMG cells can potentially serve as an important surrogate marker for estimating microglial activation in the human brain, and may provide previously unknown insights into the dynamic pathophysiology of microglia in patients with neuropsychiatric disorders. Thus, the iMG‐based technology could be used as a valuable reverse translational tool and provide new insights into the dynamic molecular pathophysiology of microglia in a wide variety of psychiatric and physical disorders.

    DOI： 10.1111/cen3.12815

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  • Engineering of Human Blood-Induced Microglia-like Cells for Reverse-Translational Brain Research. Reviewed International journal

    Sota Kyuragi, Shogo Inamine, Masahiro Ohgidani, Takahiro A Kato

    Journal of visualized experiments : JoVE   ( 211 )   2024.9

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    Language：English   Publishing type：Research paper (scientific journal)  

    Recent investigations employing animal models have highlighted the significance of microglia as crucial immunological modulators in various neuropsychiatric and physical diseases. Postmortem brain analysis and positron emission tomography imaging are representative research methods that evaluate microglial activation in human patients; the findings have revealed the activation of microglia in the brains of patients presenting with various neuropsychiatric disorders and chronic pain. Nonetheless, the aforementioned technique merely facilitates the assessment of limited aspects of microglial activation. In lieu of brain biopsy and the induced pluripotent stem cell technique, we initially devised a technique to generate directly induced microglia-like (iMG) cells from freshly derived human peripheral blood monocytes by supplementing them with granulocyte-macrophage colony-stimulating factor and interleukin 34 for 2 weeks. These iMG cells can be employed to perform dynamic morphological and molecular-level analyses concerning phagocytic capacity and cytokine releases following cellular-level stress stimulation. Recently, comprehensive transcriptome analysis has been used to verify the similarity between human iMG cells and brain primary microglia. The patient-derived iMG cells may serve as key surrogate markers for predicting microglial activation in human brains and have aided in the unveiling of previously unknown dynamic pathophysiology of microglia in patients with Nasu-Hakola disease, fibromyalgia, bipolar disorder, and Moyamoya disease. Therefore, the iMG-based technique serves as a valuable reverse-translational tool and provides novel insights into elucidating dynamic the molecular pathophysiology of microglia in a variety of mental and physical diseases.

    DOI： 10.3791/66819

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  • A high-fat diet influences neural stem and progenitor cell environment in the medulla of adult mice. Reviewed International journal

    Eriko Furube, Masahiro Ohgidani, Yusuke Tanaka, Seiji Miyata, Shigetaka Yoshida

    Neuroscience   559   64 - 76   2024.8

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    It has been widely established that neural stem cells (NSCs) exist in the adult mammalian brain. The area postrema (AP) and the ependymal cell layer of the central canal (CC) in the medulla were recently identified as NSC niches. There are two types of NSCs: astrocyte-like cells in the AP and tanycyte-like cells in the CC. However, limited information is currently available on the characteristics and functional significance of these NSCs and their progeny in the AP and CC. The AP is a part of the dorsal vagal complex (DVC), together with the nucleus of the solitary tract (Sol) and the dorsal motor nucleus of the vagus (10 N). DVC is the primary site for the integration of visceral neuronal and hormonal cues that act to inhibit food intake. Therefore, we examined the effects of high-fat diet (HFD) on NSCs and progenitor cells in the AP and CC. Eight-week-old male mice were fed HFD for short (1 week) and long periods (4 weeks). To detect proliferating cells, mice consecutively received intraperitoneal injections of BrdU for 7 days. Brain sections were processed with immunohistochemistry using various cell markers and BrdU antibodies. Our data demonstrated that adult NSCs and neural progenitor cells (NPCs) in the medulla responded more strongly to short-term HFD than to long-term HFD. HFD increased astrocyte density in the Sol and 10 N, and increased microglial/macrophage density in the AP and Sol. Furthermore, long-term HFD induced mild inflammation in the medulla, suggesting that it affected the proliferation of NSCs and NPCs.

    DOI： 10.1016/j.neuroscience.2024.08.034

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  • Heterogeneity and mitochondrial vulnerability configurate the divergent immunoreactivity of human induced microglia-like cells. Reviewed International journal

    Kousuke Yonemoto, Fumihiko Fujii, Ryoji Taira, Masahiro Ohgidani, Katsuhide Eguchi, Sayaka Okuzono, Yuko Ichimiya, Yuri Sonoda, Pin Fee Chong, Hironori Goto, Hikaru Kanemasa, Yoshitomo Motomura, Masataka Ishimura, Yuhki Koga, Keita Tsujimura, Takao Hashiguchi, Hiroyuki Torisu, Ryutaro Kira, Takahiro A Kato, Yasunari Sakai, Shouichi Ohga

    Clinical immunology (Orlando, Fla.)   255   109756 - 109756   2023.10

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    Microglia play versatile roles in progression of and protection against neuroinflammatory diseases. Little is known, however, about the mechanisms underlying the diverse reactivity of microglia to inflammatory conditions. We investigated how human induced microglia-like (iMG) cells respond to innate immune ligands. Quantitative PCR showed that poly-I:C and lipopolysaccharide (LPS) activated the expression of IL1B and TNF. Immunoreactivity of iMG did not differ between controls (n = 11) and patients with neuroinflammatory diseases (n = 24). Flow cytometry revealed that CD14high cells expressed interleukin (IL) -1β after LPS treatment. Immunoblotting showed that poly-I:C and LPS differentially activated inflammatory pathways but commonly induced mitochondrial instability and the expression of pyruvate kinase isoform M2 (PKM2). Furthermore, a potent stimulator of PKM2 (DASA-58) alleviated IL-1β production after LPS treatment. These data indicate that heterogeneous cell populations and mitochondrial stability underlie the divergent immunoreactivity of human iMG in environments.

    DOI： 10.1016/j.clim.2023.109756

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  • Angiogenic and inflammatory responses in human induced microglia-like (iMG) cells from patients with Moyamoya disease. Reviewed International journal

    Noritoshi Shirozu, Masahiro Ohgidani, Nobuhiro Hata, Shunya Tanaka, Shogo Inamine, Noriaki Sagata, Tetsuaki Kimura, Ituro Inoue, Koichi Arimura, Akira Nakamizo, Ataru Nishimura, Naoki Maehara, Soh Takagishi, Katsuma Iwaki, Tomohiro Nakao, Keiji Masuda, Yasunari Sakai, Masahiro Mizoguchi, Koji Yoshimoto, Takahiro A Kato

    Scientific reports   13 ( 1 )   14842 - 14842   2023.9

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    Angiogenic factors associated with Moyamoya disease (MMD) are overexpressed in M2 polarized microglia in ischemic stroke, suggesting that microglia may be involved in the pathophysiology of MMD; however, existing approaches are not applicable to explore this hypothesis. Herein we applied blood induced microglial-like (iMG) cells. We recruited 25 adult patients with MMD and 24 healthy volunteers. Patients with MMD were subdivided into progressive (N = 7) or stable (N = 18) group whether novel symptoms or radiographic advancement of Suzuki stage within 1 year was observed or not. We produced 3 types of iMG cells; resting, M1-, and M2-induced cells from monocytes, then RNA sequencing followed by GO and KEGG pathway enrichment analysis and qPCR assay were performed. RNA sequencing of M2-induced iMG cells revealed that 600 genes were significantly upregulated (338) or downregulated (262) in patients with MMD. Inflammation and immune-related factors and angiogenesis-related factors were specifically associated with MMD in GO analysis. qPCR for MMP9, VEGFA, and TGFB1 expression validated these findings. This study is the first to demonstrate that M2 microglia may be involved in the angiogenic process of MMD. The iMG technique provides a promising approach to explore the bioactivity of microglia in cerebrovascular diseases.

    DOI： 10.1038/s41598-023-41456-z

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  • Ameliorative effects of Fingolimod (FTY720) on microglial activation and psychosis-related behavior in short term cuprizone exposed mice. Reviewed International journal

    Siyao Li, Koki Sakurai, Masahiro Ohgidani, Takahiro A Kato, Takatoshi Hikida

    Molecular brain   16 ( 1 )   59 - 59   2023.7

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    Schizophrenia is a psychiatric disorder that affects around 1% of the population in widespread populations, with severe cases leading to long-term hospitalization and necessitation of lifelong treatment. Recent studies on schizophrenia have highlighted the involvement of inflammatory and immunoregulatory mechanisms with the onset of symptoms, and the usage of anti-inflammatory treatments are being tested against periods of rapid psychosis. In the central nervous system, microglia are the innate immune population which are activated in response to a wide range of physical and psychological stress factors and produce proinflammatory mediators such as cytokines. Microglial activation and neuroinflammation has been associated to numerous psychiatric disorders including schizophrenia, especially during psychotic episodes. Thus, novel treatments which dampen microglial activation may be of great relevance in the treatment of psychiatric disorders. Fingolimod (FTY720) is a drug used as an immunosuppressive treatment to multiple sclerosis. Recent clinical trials have focused on FTY720 as a treatment for the behavioral symptoms in schizophrenia. However, the mechanisms of Fingolimod in treating the symptoms of schizophrenia are not clear. In this study we use a recently developed neuroinflammatory psychosis model in mice: cuprizone short-term exposure, to investigate the effects of FTY720 administration. FTY720 administration was able to completely alleviate methamphetamine hypersensitivity caused by cuprizone exposure. Moreover, administration of FTY720 improved multiple measures of neuroinflammation (microglial activation, cytokine production, and leucocyte infiltration). In conclusion, our results highlight the future use of FTY720 as a direct anti-inflammatory treatment against microglial activation and psychosis.

    DOI： 10.1186/s13041-023-01047-5

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  • Systemic Inflammation Leads to Changes in the Intracellular Localization of KLK6 in Oligodendrocytes in Spinal Cord White Matter. Reviewed International journal

    Eriko Furube, Masahiro Ohgidani, Shigetaka Yoshida

    Neurochemical research   2023.4

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    Axonal injury and demyelination occur in demyelinating diseases, such as multiple sclerosis, and the detachment of myelin from axons precedes its degradation. Paranodes are the areas at which each layer of the myelin sheath adheres tightly to axons. The destruction of nodal and paranodal structures during inflammation is an important pathophysiology of various neurological disorders. However, the underlying pathological changes in these structures remain unclear. Kallikrein 6 (KLK6), a serine protease produced by oligodendrocytes, is involved in demyelinating diseases. In the present study, we intraperitoneally injected mice with LPS for several days and examined changes in the localization of KLK6. Transient changes in the intracellular localization of KLK6 to paranodes in the spinal cord were observed during LPS-induced systemic inflammation. However, these changes were not detected in the upper part of brain white matter. LPS-induced changes were suppressed by minocycline, suggesting the involvement of microglia. Moreover, nodal lengths were elongated in LPS-treated wild-type mice, but not in LPS-treated KLK6-KO mice. These results demonstrate the potential involvement of KLK6 in the process of demyelination.

    DOI： 10.1007/s11064-023-03929-5

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  • Neurotoxicity Assessment System for Metals Using Mixed Cultures of Neural and Glial Cell Lines Reviewed

    Ohgidani Masahiro, Furube Eriko, Tanaka Yusuke, Yoshida Shigetaka

    Alternatives to Animal Testing and Experimentation   28 ( 1 )   8 - 14   2023

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    Authorship：Lead author,　Corresponding author   Language：English   Publisher：Japanese Society for Alternative to Animal Experiments  

    Evaluations of the toxicity of hazardous substances in foods and other products are essential. Metals are severely neurotoxic to humans. To date, neurotoxicity has mainly been examined in animal experiments using rodents; however, the importance of using <i>in vitro</i> systems has recently been reported. Although the brain also contains glial cells, <i>in vitro</i> assessments of neurotoxicity have mainly been performed using neurons. Therefore, we established a high-throughput evaluation system by creating a mixed culture system of microglia, a type of glial cell, and neurons using BV2 and Neuro2A cells. The mixed culture showed changes in gene expression compared to the monoculture. Furthermore, in examinations of the toxicities of various metals, some exhibited different toxicities in the mixed culture from those in the single culture. These results suggest that the conventional evaluation system using single cultures is insufficient and also that the use of glial cells to accurately assess neurotoxicity may be necessary.

    DOI： 10.11232/aatex.28.8

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  • A case of bipolar disorder with <i>AIF1</i> (coding gene of Iba‐1) deletion: A pilot <i>in vitro</i> analysis using blood‐derived microglia‐like cells Reviewed

    Masahiro Ohgidani, Itaru Kushima, Shogo Inamine, Sota Kyuragi, Noriaki Sagata, Tomohiro Nakao, Shigenobu Kanba, Norio Ozaki, Takahiro A Kato

    Psychiatry and Clinical Neurosciences   77 ( 2 )   128 - 130   2022.11

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    Authorship：Lead author   Publishing type：Research paper (scientific journal)   Publisher：Wiley  

    DOI： 10.1111/pcn.13505

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    Other Link： https://onlinelibrary.wiley.com/doi/full-xml/10.1111/pcn.13505

  • Preliminary analysis of hippocampus synaptic apoptosis and microglial phagocytosis induced by severe restraint stress Reviewed

    Shingo Enomoto, Masahiro Ohgidani, Noriaki Sagata, Shogo Inamine, Takahiro A. Kato

    Neuropsychopharmacology Reports   43 ( 1 )   120 - 125   2022.11

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    Authorship：Lead author   Publishing type：Research paper (scientific journal)   Publisher：Wiley  

    DOI： 10.1002/npr2.12298

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    Other Link： https://onlinelibrary.wiley.com/doi/full-xml/10.1002/npr2.12298

  • Effect of memantine, an anti-Alzheimer’s drug, on rodent microglial cells in vitro Reviewed

    Toru Murakawa-Hirachi, Yoshito Mizoguchi, Masahiro Ohgidani, Yoshinori Haraguchi, Akira Monji

    Scientific Reports   11 ( 1 )   2021.12

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    DOI： 10.1038/s41598-021-85625-4

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  • Plasma acetylcholine and nicotinic acid are correlated with focused preference for photographed females in depressed males: an economic game study Reviewed

    Hiroaki Kubo, Daiki Setoyama, Motoki Watabe, Masahiro Ohgidani, Kohei Hayakawa, Nobuki Kuwano, Mina Sato-Kasai, Ryoko Katsuki, Shigenobu Kanba, Dongchon Kang, Takahiro A. Kato

    Scientific Reports   11 ( 1 )   2021.12

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    DOI： 10.1038/s41598-020-75115-4

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  • CD206 Expression in Induced Microglia-Like Cells From Peripheral Blood as a Surrogate Biomarker for the Specific Immune Microenvironment of Neurosurgical Diseases Including Glioma Reviewed

    Shunya Tanaka, Masahiro Ohgidani, Nobuhiro Hata, Shogo Inamine, Noriaki Sagata, Noritoshi Shirouzu, Nobutaka Mukae, Satoshi O. Suzuki, Hideomi Hamasaki, Ryusuke Hatae, Yuhei Sangatsuda, Yutaka Fujioka, Kosuke Takigawa, Yusuke Funakoshi, Toru Iwaki, Masako Hosoi, Koji Iihara, Masahiro Mizoguchi, Takahiro A. Kato

    Frontiers in Immunology   12   2021.6

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    Authorship：Lead author   Publishing type：Research paper (scientific journal)   Publisher：Frontiers Media SA  

    Targeting the unique glioma immune microenvironment is a promising approach in developing breakthrough immunotherapy treatments. However, recent advances in immunotherapy, including the development of immune checkpoint inhibitors, have not improved the outcomes of patients with glioma. A way of monitoring biological activity of immune cells in neural tissues affected by glioma should be developed to address this lack of sensitivity to immunotherapy. Thus, in this study, we sought to examine the feasibility of non-invasive monitoring of glioma-associated microglia/macrophages (GAM) by utilizing our previously developed induced microglia-like (iMG) cells. Primary microglia (pMG) were isolated from surgically obtained brain tissues of 22 patients with neurological diseases. iMG cells were produced from monocytes extracted from the patients’ peripheral blood. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) revealed a significant correlation of the expression levels of representative markers for M1 and M2 microglia phenotypes between pMG and the corresponding iMG cells in each patient (Spearman’s correlation coefficient = 0.5225, <italic>P &amp;lt;</italic>0.0001). Synchronous upregulation of CD206 expression levels was observed in most patients with glioma (6/9, 66.7%) and almost all patients with glioblastoma (4/5, 80%). Therefore, iMG cells can be used as a minimally invasive tool for monitoring the disease-related immunological state of GAM in various brain diseases, including glioma. CD206 upregulation detected in iMG cells can be used as a surrogate biomarker of glioma.

    DOI： 10.3389/fimmu.2021.670131

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  • Personality classification enhances blood metabolome analysis and biotyping for major depressive disorders: two-species investigation Reviewed

    Daiki Setoyama, Atsuo Yoshino, Masahiro Takamura, Go Okada, Masaaki Iwata, Kyohei Tsunetomi, Masahiro Ohgidani, Nobuki Kuwano, Junichiro Yoshimoto, Yasumasa Okamoto, Shigeto Yamawaki, Shigenobu Kanba, Dongchon Kang, Takahiro A. Kato

    Journal of Affective Disorders   279   20 - 30   2021.1

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    DOI： 10.1016/j.jad.2020.09.118

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  • Modulation of inflammatory responses by fractalkine signaling in microglia. Reviewed International journal

    Koichi Inoue, Hiroyuki Morimoto, Masahiro Ohgidani, Takatoshi Ueki

    PloS one   16 ( 5 )   e0252118   2021

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    Reactive microglia are suggested to be involved in neurological disorders, and the mechanisms underlying microglial activity may provide insights into therapeutic strategies for neurological diseases. Microglia produce immunological responses to various stimuli, which include fractalkine (FKN or CX3CL1). CX3CR1, a FKN receptor, is present in microglial cells, and when FKN is applied before lipopolysaccharide (LPS) administration, LPS-induced inflammatory responses are inhibited, suggesting that the activation of the FKN signal is beneficial. Considering the practical administration for treatment, we investigated the influence of FKN on immunoreactive microglia using murine primary microglia and BV-2, a microglial cell line. The administration of LPS leads to nitric oxide (NO) production. NO was reduced when FKN was administered 4 h after LPS administration without a change in inducible nitric oxide synthase expression. In contrast, morphological changes, migratory activity, and proliferation were not altered by delayed FKN treatment. LPS decreases the CX3CR1 mRNA concentration, and the overexpression of CX3CR1 restores the FKN-mediated decrease in NO. CX3CR1 overexpression decreased the NO production that is mediated by LPS even without the application of FKN. ATP and ethanol also reduced CX3CR1 mRNA concentrations. In conclusion, the delayed FKN administration modified the LPS-induced microglial activation. The FKN signals were attenuated by a reduction in CX3CR1 by some inflammatory stimuli, and this modulated the inflammatory response of microglial cells, at least partially.

    DOI： 10.1371/journal.pone.0252118

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  • ProBDNF induces sustained elevation of intracellular Ca<sup>2+</sup> possibly mediated by TRPM7 channels in rodent microglial cells Reviewed

    Yoshito Mizoguchi, Masahiro Ohgidani, Yoshinori Haraguchi, Toru Murakawa-Hirachi, Takahiro A. Kato, Akira Monji

    GLIA   2021

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    Authorship：Lead author   Publishing type：Research paper (scientific journal)  

    DOI： 10.1002/glia.23996

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  • Forskolin rapidly enhances neuron-like morphological change of directly induced-neuronal cells from neurofibromatosis type 1 patients Reviewed

    Noriaki Sagata, Shin ichi Kano, Masahiro Ohgidani, Shogo Inamine, Yasunari Sakai, Hiroki Kato, Keiji Masuda, Takeshi Nakahara, Makiko Nakahara-Kido, Shouichi Ohga, Masutaka Furue, Akira Sawa, Shigenobu Kanba, Takahiro A. Kato

    Neuropsychopharmacology Reports   40 ( 4 )   396 - 400   2020.12

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    DOI： 10.1002/npr2.12144

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  • GNAO1 organizes the cytoskeletal remodeling and firing of developing neurons Reviewed

    Satoshi Akamine, Sayaka Okuzono, Hiroyuki Yamamoto, Daiki Setoyama, Noriaki Sagata, Masahiro Ohgidani, Takahiro A. Kato, Tohru Ishitani, Hiroki Kato, Keiji Masuda, Yuki Matsushita, Hiroaki Ono, Yoshito Ishizaki, Masafumi Sanefuji, Hirotomo Saitsu, Naomichi Matsumoto, Dongchon Kang, Shigenobu Kanba, Yusaku Nakabeppu, Yasunari Sakai, Shouichi Ohga

    FASEB Journal   34 ( 12 )   16601 - 16621   2020.12

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    DOI： 10.1096/fj.202001113R

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  • Antidepressant effect of the translocator protein antagonist ONO-2952 on mouse behaviors under chronic social defeat stress Reviewed International journal

    Kanako Nozaki, Hikaru Ito, Masahiro Ohgidani, Yosuke Yamawaki, Ezgi Hatice Sahin, Takashi Kitajima, Seishi Katsumata, Shigeto Yamawaki, Takahiro A. Kato, Hidenori Aizawa

    Neuropharmacology   162   107835 - 107835   2020.1

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    DOI： 10.1016/j.neuropharm.2019.107835

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  • Cuprizone-treated mice, a possible model of schizophrenia, highlighting the simultaneous abnormalities of GABA, serine and glycine in hippocampus Reviewed

    Eisuke Hayakawa, Masahiro Ohgidani, Yoshinori Fujimura, Shigenobu Kanba, Daisuke Miura, Takahiro A. Kato

    Schizophrenia Research   210   326 - 328   2019.8

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  • Suicide and microglia: Recent findings and future perspectives based on human studies Reviewed

    Hisaomi Suzuki, Masahiro Ohgidani, Nobuki Kuwano, Fabrice Chrétien, Geoffroy Lorin de la Grandmaison, Mitsumoto Onaya, Itaru Tominaga, Daiki Setoyama, Dongchon Kang, Masaru Mimura, Shigenobu Kanba, Takahiro A. Kato

    Frontiers in Cellular Neuroscience   13   1 - 10   2019.1

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    Authorship：Lead author  

    DOI： 10.3389/fncel.2019.00031

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  • Neuron-related blood inflammatory markers as an objective evaluation tool for major depressive disorder: An exploratory pilot case-control study. Reviewed

    Kuwano N, Kato TA, Mitsuhashi M, Sato-Kasai M, Shimokawa N, Hayakawa K, Ohgidani M, Sagata N, Kubo H, Sakurai T, Kanba S

    Journal of affective disorders   240   88 - 98   2018.11

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  • Tryptophan-kynurenine and lipid related metabolites as blood biomarkers for first-episode drug-naïve patients with major depressive disorder: An exploratory pilot case-control study Reviewed

    Nobuki Kuwano, Takahiro A. Kato, Daiki Setoyama, Mina Sato-Kasai, Norihiro Shimokawa, Kohei Hayakawa, Masahiro Ohgidani, Noriaki Sagata, Hiroaki Kubo, Junji Kishimoto, Dongchon Kang, Shigenob Kanba

    Journal of Affective Disorders   231   74 - 82   2018.4

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    Language：English   Publishing type：Research paper (scientific journal)   Publisher：Elsevier B.V.  

    DOI： 10.1016/j.jad.2018.01.014

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  • p66Shc Signaling Mediates Diabetes-Related Cognitive Decline. Reviewed International journal

    Yohei Minami, Noriyuki Sonoda, Eiichi Hayashida, Hiroaki Makimura, Makoto Ide, Noriko Ikeda, Masahiro Ohgidani, Takahiro A Kato, Yoshihiro Seki, Yasutaka Maeda, Shigenobu Kanba, Ryoichi Takayanagi, Yoshihiro Ogawa, Toyoshi Inoguchi

    Scientific reports   8 ( 1 )   3213 - 3213   2018.2

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    Accumlating evidence have suggested that diabetes mellitus links dementia, notably of Alzheimer's disease (AD). However, the underlying mechanism remains unclear. Several studies have shown oxidative stress (OS) to be one of the major factors in the pathogenesis of diabetic complications. Here we show OS involvement in brain damage in a diabetic animal model that is at least partially mediated through an AD-pathology-independent mechanism apart from amyloid-β accumulation. We investigated the contribution of the p66Shc signaling pathway to diabetes-related cognitive decline using p66Shc knockout (-/-) mice. p66Shc (-/-) mice have less OS in the brain and are resistant to diabetes-induced brain damage. Moreover, p66Shc (-/-) diabetic mice show significantly less cognitive dysfunction and decreased levels of OS and the numbers of microglia. This study postulates a p66Shc-mediated inflammatory cascade leading to OS as a causative pathogenic mechanism in diabetes-associated cognitive impairment that is at least partially mediated through an AD-pathology-independent mechanism.

    DOI： 10.1038/s41598-018-21426-6

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  • Blood biomarkers of Hikikomori, a severe social withdrawal syndrome. Reviewed International journal

    Kohei Hayakawa, Takahiro A Kato, Motoki Watabe, Alan R Teo, Hideki Horikawa, Nobuki Kuwano, Norihiro Shimokawa, Mina Sato-Kasai, Hiroaki Kubo, Masahiro Ohgidani, Noriaki Sagata, Hiroyuki Toda, Masaru Tateno, Naotaka Shinfuku, Junji Kishimoto, Shigenobu Kanba

    Scientific reports   8 ( 1 )   2884 - 2884   2018.2

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    Hikikomori, a severe form of social withdrawal syndrome, is a growing social issue in Japan and internationally. The pathophysiology of hikikomori has not yet been elucidated and an effective treatment remains to be established. Recently, we revealed that avoidant personality disorder is the most common comorbidity of hikikomori. Thus, we have postulated that avoidant personality is the personality underpinning hikikomori. First, we herein show relationships between avoidant personality traits, blood biomarkers, hikikomori-related psychological features, and behavioural characteristics assessed by a trust game in non-hikikomori volunteers. Avoidant personality traits were negatively associated with high-density lipoprotein cholesterol (HDL-C) and uric acid (UA) in men, and positively associated with fibrin degeneration products (FDP) and high sensitivity C-reactive protein (hsCRP) in women. Next, we recruited actual individuals with hikikomori, and compared avoidant personality traits, blood biomarkers, and psychological features between individuals with hikikomori and age-matched healthy controls. Individuals with hikikomori had higher avoidant personality scores in both sexes, and showed lower serum UA levels in men and lower HDL-C levels in women compared with healthy controls. This is the first report showing possible blood biomarkers for hikikomori, and opens the door to clarify the underlying biological pathophysiology of hikikomori.

    DOI： 10.1038/s41598-018-21260-w

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  • Modulating microglial activation as a possible therapeutic target for depression Reviewed

    Mina Sato-Kasai, Takahiro A. Kato, Masahiro Ohgidani, Hideki Horikawa, Yoshito Mizoguchi, Akira Monji, Shigenobu Kanba

    Understanding Depression   1   209 - 219   2018.1

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    DOI： 10.1007/978-981-10-6580-4_18

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  • Donepezil suppresses intracellular Ca2+ mobilization through the PI3K pathway in rodent microglia Reviewed

    Yoshinori Haraguchi, Yoshito Mizoguchi, Masahiro Ohgidani, Yoshiomi Imamura, Toru Murakawa-Hirachi, Hiromi Nabeta, Hiroshi Tateishi, Takahiro A. Kato, Akira Monji

    JOURNAL OF NEUROINFLAMMATION   14 ( 1 )   258   2017.12

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    DOI： 10.1186/s12974-017-1033-0

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  • Dysregulated gene expressions of MEX3D, FOS and BCL2 in human induced-neuronal (iN) cells from NF1 patients: a pilot study Reviewed

    Noriaki Sagata, Takahiro A. Kato, Shin-ichi Kano, Masahiro Ohgidani, Norihiro Shimokawa, Mina Sato-Kasai, Kohei Hayakawa, Nobuki Kuwano, Ashley M. Wilson, Koko Ishizuka, Shiori Kato, Takeshi Nakahara, Makiko Nakahara-Kido, Daiki Setoyama, Yasunari Sakai, Shouichi Ohga, Masutaka Furue, Akira Sawa, Shigenobu Kanba

    SCIENTIFIC REPORTS   7 ( 1 )   13905   2017.10

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    DOI： 10.1038/s41598-017-14440-7

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  • Fibromyalgia and microglial TNF-alpha: Translational research using human blood induced microglia-like cells Reviewed

    Masahiro Ohgidani, Takahiro A. Kato, Masako Hosoi, Makoto Tsuda, Kohei Hayakawa, Chie Hayaki, Rie Iwaki, Noriaki Sagata, Ryota Hashimoto, Kazuhide Inoue, Nobuyuki Sudo, Shigenobu Kanba

    SCIENTIFIC REPORTS   7 ( 1 )   11882   2017.9

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    DOI： 10.1038/s41598-017-11506-4

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  • Translational research on neuropsychiatrie disorders: Focusing on microglia hypothesis Reviewed

    Takahiro A. Kato, Masahiro Ohgidani, Shigenobu Kanba

    Brain and Nerve   69 ( 9 )   1007 - 1015   2017.9

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  • Microglia-derived neuregulin expression in psychiatric disorders. Reviewed International journal

    Daisuke Ikawa, Manabu Makinodan, Keiko Iwata, Masahiro Ohgidani, Takahiro A Kato, Yasunori Yamashita, Kazuhiko Yamamuro, Sohei Kimoto, Michihiro Toritsuka, Takahira Yamauchi, Shin-Ichi Fukami, Hiroki Yoshino, Kazuki Okumura, Tatsuhide Tanaka, Akio Wanaka, Yuji Owada, Masatsugu Tsujii, Toshiro Sugiyama, Kenji Tsuchiya, Norio Mori, Ryota Hashimoto, Hideo Matsuzaki, Shigenobu Kanba, Toshifumi Kishimoto

    Brain, behavior, and immunity   61   375 - 385   2017.3

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    DOI： 10.1016/j.bbi.2017.01.003

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  • Microglial CD206 Gene Has Potential as a State Marker of Bipolar Disorder Reviewed

    Masahiro Ohgidani, Takahiro A. Kato, Yoshinori Haraguchi, Toshio Matsushima, Yoshito Mizoguchi, Toru Murakawa-Hirachi, Noriaki Sagata, Akira Monji, Shigenobu Kanba

    FRONTIERS IN IMMUNOLOGY   7   676   2017.1

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    DOI： 10.3389/fimmu.2016.00676

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  • Plasma Metabolites Predict Severity of Depression and Suicidal Ideation in Psychiatric Patients-A Multicenter Pilot Analysis Reviewed

    Daiki Setoyama, Takahiro A. Kato, Ryota Hashimoto, Hiroshi Kunugi, Kotaro Hattori, Kohei Hayakawa, Mina Sato-Kasai, Norihiro Shimokawa, Sachie Kaneko, Sumiko Yoshida, Yu-ichi Goto, Yuka Yasuda, Hidenaga Yamamori, Masahiro Ohgidani, Noriaki Sagata, Daisuke Miura, Dongchon Kang, Shigenobu Kanba

    PLOS ONE   11 ( 12 )   e0165267   2016.12

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    DOI： 10.1371/journal.pone.0165267

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  • Aripiprazole inhibits polyI: C-induced microglial activation possibly via TRPM7 Reviewed

    Mina Sato-Kasai, Takahiro A. Kato, Masahiro Ohgidani, Yoshito Mizoguchi, Noriaki Sagata, Shogo Inamine, Hideki Horikawa, Kohei Hayakawa, Norihiro Shimokawa, Sota Kyuragi, Yoshihiro Seki, Akira Monji, Shigenobu Kanba

    SCHIZOPHRENIA RESEARCH   178 ( 1-3 )   35 - 43   2016.12

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    DOI： 10.1016/j.schres.2016.08.022

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  • TNF-alpha from hippocampal microglia induces working memory deficits by acute stress in mice Reviewed

    Masahiro Ohgidani, Takahiro A. Kato, Noriaki Sagata, Kohei Hayakawa, Norihiro Shimokawa, Mina Sato-Kasai, Shigenobu Kanba

    BRAIN BEHAVIOR AND IMMUNITY   55   17 - 24   2016.7

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    DOI： 10.1016/j.bbi.2015.08.022

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  • Directly Induced Glial/Neuronal Cells from Human Peripheral Tissues: A Novel Translational Research Tool for Neuropsychiatric Disorders Reviewed

    Takahiro A. Kato, Masahiro Ohgidani, Noriaki Sagata, Shigenobu Kanba

    Advances in Neuroimmune Biology   6 ( 2 )   95 - 105   2016

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  • Introducing directly induced microglia-like (iMG) cells from fresh human monocytes: a novel translational research tool for psychiatric disorders Reviewed

    Masahiro Ohgidani, Takahiro A. Kato, Shigenobu Kanba

    FRONTIERS IN CELLULAR NEUROSCIENCE   9   184   2015.5

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    DOI： 10.3389/fncel.2015.00184

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  • Brain-derived Neurotrophic Factor (BDNF) Induces Sustained Intracellular Ca2+ Elevation through the Up-regulation of Surface Transient Receptor Potential 3 (TRPC3) Channels in Rodent Microglia Reviewed

    Yoshito Mizoguchi, Takahiro A. Kato, Yoshihiro Seki, Masahiro Ohgidani, Noriaki Sagata, Hideki Horikawa, Yusuke Yamauchi, Mina Sato-Kasai, Kohei Hayakawa, Ryuji Inoue, Shigenobu Kanba, Akira Monji

    JOURNAL OF BIOLOGICAL CHEMISTRY   289 ( 26 )   18549 - 18555   2014.6

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    DOI： 10.1074/jbc.M114.555334

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  • Direct induction of ramified microglia-like cells from human monocytes: Dynamic microglial dysfunction in Nasu-Hakola disease Reviewed

    Masahiro Ohgidani, Takahiro A. Kato, Daiki Setoyama, Noriaki Sagata, Ryota Hashimoto, Kazue Shigenobu, Tetsuhiko Yoshida, Kohei Hayakawa, Norihiro Shimokawa, Daisuke Miura, Hideo Utsumi, Shigenobu Kanba

    SCIENTIFIC REPORTS   4   4957   2014.5

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    DOI： 10.1038/srep04957

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  • Block/homo polyplex micelle-based GM-CSF gene therapy via intraperitoneal administration elicits antitumor immunity against peritoneal dissemination and exhibits safety potentials in mice and cynomolgus monkeys Reviewed

    Masahiro Ohgidani, Koichi Furugaki, Kentaro Shinkai, Yumi Kunisawa, Keiji Itaka, Kazunori Kataoka, Kenji Nakano

    JOURNAL OF CONTROLLED RELEASE   167 ( 3 )   238 - 247   2013.5

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    DOI： 10.1016/j.jconrel.2013.02.006

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  • Residual powders from Shochu distillation remnants induce apoptosis in human hepatoma cells via the caspase-independent pathway Reviewed

    Masahiro Ohgidani, Yuji Komizu, Koichi Goto, Ryuichi Ueoka

    JOURNAL OF BIOSCIENCE AND BIOENGINEERING   114 ( 1 )   104 - 109   2012.7

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    DOI： 10.1016/j.jbiosc.2012.02.026

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  • Antimelanogenic and antioxidative effects of residual powders from Shochu distillation remnants Reviewed

    Masahiro Ohgidani, Yuji Komizu, Koichi Goto, Ryuichi Ueoka

    FOOD CHEMISTRY   132 ( 4 )   2140 - 2143   2012.6

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    DOI： 10.1016/j.foodchem.2011.12.049

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  • Anticancer Effects of Residual Powder from Barley-Shochu Distillation Remnants against the Orthotopic Xenograft Mouse Models of Hepatocellular Carcinoma in Vivo Reviewed

    Masahiro Ohgidani, Hideaki Ichihara, Koichi Goto, Yoko Matsumoto, Ryuichi Ueoka

    BIOLOGICAL & PHARMACEUTICAL BULLETIN   35 ( 6 )   984 - 987   2012.6

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    DOI： 10.1248/bpb.35.984

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MISC

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Presentations

  • グリア細胞からアプローチする生物学的精神医学研究 Invited

    扇谷 昌宏

    第21回日本うつ病学会総会  2024 

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  • ヒト末梢血誘導型ミクログリア細胞技術を用いた慢性疼痛研究 Invited

    扇谷 昌宏

    第62回日本心身医学会総会学術講演会  2021 

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  • Introducing our psychiatric translational reserch system to clarify the pathological neuron-glia interaction using human induced microglia-like (iMG) cells and induced neuronal (iN) cells. Invited

    Masahiro Ohgidani

    6th Congress of Asian College of Neuropsychopharmacology  2019.10 

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  • ヒト血液由来ミクログリア様細胞を用いた線維筋痛症の客観的バイオマーカー開発 Invited

    扇谷昌宏, 加藤隆弘

    第35回日本ストレス学会学術総会  2019 

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Industrial property rights

Awards

  • 優秀論文賞

    2024.11   日本動物実験代替法学会  

    扇谷 昌宏

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  • JSNP Excellent Presentation Award for CINP 2024

    2024.5   Japanese Society of Neuropsychhopharmacology   Direct induction of microglia-like cells from human monocytes: A novel cellular tool for translational research of neuropsychoiatric disorders

    Masahiro Ohgidani

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  • 優秀発表賞

    2019.10   日本神経精神薬理学会   第49回日本精神神経薬理学会年会

    扇谷昌宏

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  • 若手優秀発表賞

    2019.7   日本神経化学会   第62回日本神経化学会、第42回日本神経科学会合同大会

    扇谷昌宏

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  • 奨励賞

    2018.6   日本生物学的精神医学会   第41回日本生物学的精神医学会

    扇谷昌宏

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  • 優秀演題賞

    2017.11   日本動物実験代替法学会   日本動物実験代替法学会第31回大会

    扇谷昌宏

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  • KJYPA award

    2016.11   Korea-Japan Young Psychiatrists’ Conference   18th Korea-Japan Young Psychiatrists’ Conference.

    Masahiro Ohgidani

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  • 学会年会賞

    2015.7   日本神経精神薬理学会   第46回日本神経精神薬理学会年会

    扇谷昌宏

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  • 優秀賞

    2010.12   大学発ベンチャービジネスプランコンテスト実行委員会   第10回大学発ベンチャービジネスプランコンテスト

    扇谷昌宏

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  • 奨励賞

    2009.11   熊本県   夢挑戦ビジネス大賞2009 in くまもと

    扇谷昌宏

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Research Projects

  • ヒトの末梢及び中枢免疫系から明らかにする加齢の正体と加齢性疾患治療への応用

    Grant number：24K22242  2024.6 - 2026.3

    日本学術振興会  科学研究費助成事業  挑戦的研究(萌芽)

    扇谷 昌宏

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    Authorship：Principal investigator 

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  • 精神神経疾患におけるミクログリア活性化とは何か？ヒト細胞を用いた疾患横断的研究

    Grant number：23K24261  2024.4 - 2025.3

    日本学術振興会  科学研究費助成事業  基盤研究(B)

    扇谷 昌宏, 山崎 亮, 加藤 隆弘

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  • ヒト末梢血誘導型ミクログリア細胞（iMG）技術を用いた認知症の病態機序解析ならびに臨床症状と細胞機能との相互解析による新規治療標的の探索

    2022.4 - 2025.3

    日本医療研究開発機構(AMED)  認知症研究開発事業 

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  • What is microglial activation in neuropsychiatric disorders? A cross-disease study using human cells.

    Grant number：22H03000  2022.4 - 2025.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (B)  Grant-in-Aid for Scientific Research (B)

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  • dynamic analysis in induced-microglial cells from patients with major depression disorder and obstructive sleep apnea syndrome before and after treated with continuous positive airway pressure therapy

    Grant number：21K07523  2021.4 - 2024.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)  Grant-in-Aid for Scientific Research (C)

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    Authorship：Coinvestigator(s) 

    Grant amount：\4,290,000 （ Direct Cost: \3,300,000 、 Indirect Cost：\990,000 ）

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  • Pathophysiology of cognitive dysfunction in schizophrenia focusing on the hypothesis of accelerated cerebral aging by CCL11

    Grant number：21H02845  2021.4 - 2024.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (B)

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  • Elucidation of glioma immune microenvironment heterogeneity based on immunogenomics by liquid biopsy

    Grant number：21H03044  2021.4 - 2024.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (B)  Grant-in-Aid for Scientific Research (B)

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    Authorship：Coinvestigator(s) 

    Grant amount：\17,550,000 （ Direct Cost: \13,500,000 、 Indirect Cost：\4,050,000 ）

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  • ヒト末梢血誘導型ミクログリア細胞技術を用いた食品の神経毒性評価システムの開発

    2020.4 - 2023.3

    厚生労働省  厚生労働科学研究費補助金 

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  • Elucidation of the pathomechanisms of microglial diseases with severe neuropsychiatric symptoms and search for treatment options.

    Grant number：19K17065  2019.4 - 2022.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Early-Career Scientists

    Ohgidani Masahiro

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    Grant amount：\4,160,000 （ Direct Cost: \3,200,000 、 Indirect Cost：\960,000 ）

    Microglia play various roles in the brain, and their dysfunction causes microglial disease, which presents with severe neuropsychiatric symptoms. This study aims to analyze microglial dysfunctions at the cellular level using the human peripheral blood-induced microglia-like cell technology developed by the applicant, to elucidate the pathomechanisms of microglial diseases and to search for novel therapeutic strategies.
    As a result of this research, blood samples were taken from actual HDLS patients, and analysis of the microglia-like cells produced revealed that they were different compared to healthy subjects. In addition, they found similar changes in clinical samples in microglial cells from mouse brains and in model cells generated using siRNA. The paper is currently being submitted for publication.

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  • dynamic state analysis in induced-microglial cells from delirium population and non-delirium population

    Grant number：19K08022  2019.4 - 2022.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)  Grant-in-Aid for Scientific Research (C)

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    Authorship：Coinvestigator(s) 

    Grant amount：\4,290,000 （ Direct Cost: \3,300,000 、 Indirect Cost：\990,000 ）

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  • Establishment of objective evaluation system for chronic fatigue syndrome using human peripheral blood induced microglia-like cells

    Grant number：17K19915  2017.6 - 2019.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Challenging Research (Exploratory)  Grant-in-Aid for Challenging Research (Exploratory)

    Ohgidani Masahiro

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    Authorship：Principal investigator 

    Grant amount：\6,370,000 （ Direct Cost: \4,900,000 、 Indirect Cost：\1,470,000 ）

    The aim of this study was to develop an objective evaluation method for the involvement of microglia in chronic fatigue syndrome using the peripheral blood derived microglia-like cell technology.
    In a group of fibromyalgia patients with symptoms similar to those of chronic fatigue syndrome, TNF-α gene expression was significantly increased after ATP stimulation. More interestingly, there was a positive correlation between the severity of anxiety and depression (HAD) and the expression level of the TNF-α gene. These findings suggest that psychiatric symptoms in the patient population may be controlled by microglia-derived TNF-α.

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  • Establishment of humani microglial cells and application to psychiatric disorders

    Grant number：26860933  2014.4 - 2017.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Young Scientists (B)  Grant-in-Aid for Young Scientists (B)

    Ohgidani Masahiro

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    Grant amount：\3,770,000 （ Direct Cost: \2,900,000 、 Indirect Cost：\870,000 ）

    ・It was succeeded that establishment of human microglia-like cells from monocyte.
    ・Abnormality of microglial function was observed in microglilal disease including psychiatric disorders.
    ・It was suggested that this technique will be useful for future microglial studies.

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