Updated on 2025/12/09

写真a

 
MITANI Tomoki
 
Organization
Brain Research Institute Center for Integrated Human Brain Science Department of Functional Neurology and Neurosurgery Specially Appointed Assistant Professor
Title
Specially Appointed Assistant Professor
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Degree

  • M.D. Ph.D ( 2025.3   Osaka University )

Research Areas

  • Informatics / Mathematical informatics

  • Life Science / Anatomy and histopathology of nervous system

  • Life Science / Neuroscience-general

  • Life Science / Human pathology

  • Natural Science / Biophysics, chemical physics and soft matter physics

  • Life Science / Biophysics

  • Life Science / Molecular biology

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Research History (researchmap)

  • The University of Tokyo   Graduate School of Medicine

    2025.4

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    Country：Japan

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  • Niigata University   Brain Research Institute Center for Integrated Human Brain Science   Assistant Professor

    2025.4

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    Country：Japan

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  • 国立研究開発法人科学技術振興機構 (JST) ACT-X 研究者

    2024.10

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  • Osaka University   Graduate School of Medicine   Guest Lecturer

    2021.4

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    Country：Japan

    Notes：Department of Neurology

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  • Graduate School of Medicine   PhD student

    2021.4 - 2025.3

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  • RIKEN Center for Biosystems Dynamics Research (BDR)   Laboratory for Synthetic Biology   Research Fellow

    2019.4 - 2025.3

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  • Osaka University Hospital, Osaka, Japan   Resident

    2019.4 - 2021.3

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  • RIKEN Quantitative Biology Center (QBiC)   Laboratory for Synthetic Biology   Student Trainee

    2015.4 - 2019.3

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  • Graduate School of Medicine, Osaka University   Department of RNA Biology and Neuroscience   MD-researcher program

    2013.12 - 2015.3

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  • B.A. in Medicine, Osaka University, Osaka, Japan

    2013.4 - 2019.3

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  • 三重県私立高田高校

    2010.4 - 2013.3

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Research History

  • Niigata University   Department of Functional Neurology and Neurosurgery, Center for Integrated Human Brain Science, Brain Research Institute   Specially Appointed Assistant Professor

    2025.4

  • Osaka University   Graduate student(doctorate program)

    2021.4 - 2025.3

Professional Memberships

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Papers

  • A whole-brain single-cell atlas of circadian neural activity in mice

    Seiji Okada, Hiroki R. Ueda, Hiroshi Fujishima, Katsunari Yamashita, Fukuaki Lee Kinoshita, Shota Y Yoshida, Katsuhiko Matsumoto, Tomoki T Mitani, Yoichi Minami, Rikuhiro G Yamada, Eiichi Morii

    Science   2025.11

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    Publishing type：Research paper (scientific journal)  

    DOI： 10.1126/science.aea3381

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  • Whole-Brain Single-Neuron Atlas Reveals Microglial Security Hole Accelerating Neuronal Vulnerability

    Tomoki Mitani, Kosei Yamaura, Rikuhiro Yamada, Katsuhiko Matsumoto, Etsuo Susaki, Naruhiko Sahara, Rin Yanai, Kensuke Ikenaka, Shiying Jiang, Hideki Hayakawa, Hideki Mochizuki, Kousuke Baba, Hiroki Ueda

    Preprint (Research Square)   2025.2

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    Authorship：Lead author   Publisher：Springer Science and Business Media LLC  

    Abstract <p>Neurodegenerative diseases are characterized by progressive neuronal loss, yet subtle degeneration remains difficult to detect, hindering advancements in early diagnosis and intervention strategies. Here, we present a 3D, whole-brain, single-neuron atlas that aligns and compares neurons at single-cell resolution, surpassing 2D spatial limitations to precisely detect heterogeneous neurodegenerative lesions. Using the AppNL-G-F model of Alzheimer’s disease, we found that neuronal loss begins concurrently with amyloid-β deposition, indicating a more acute timeline than proposed by the amyloid hypothesis. We also identified age-dependent microglial redistribution from gray-matter–rich to white-matter–rich regions in wild-type mice, accelerated in AppNL-G-F, potentially reducing neuroprotective function. Spatial single-cell-resolution risk analysis revealed microglial depletion, rather than proliferation, as an early risk indicator for neuronal loss, and microgliosis often coexists with microglial loss, suggesting heightened microglial vulnerability. Integration with spatial transcriptomics showed neurons near microglia with reduced homeostatic gene expression are especially vulnerable. Together, these findings demonstrated that amyloid pathology skews microglial distribution and promotes their exhaustion, leading to microglial spatial disorganization and neuronal vulnerability, resulting in “microglial security holes”. Our study underscores the transformative potential of 3D analysis in neurodegenerative research, offering a versatile platform for organ-level spatial multi-omics integration to advance detection and therapeutic strategies.</p>

    DOI： 10.21203/rs.3.rs-5827312/v1

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    Other Link： https://www.researchsquare.com/article/rs-5827312/v1.html

  • DECODE enables high-throughput mapping of antibody epitopes at single amino acid resolution. Reviewed International journal

    Katsuhiko Matsumoto, Shoko Y Harada, Shota Y Yoshida, Ryohei Narumi, Tomoki T Mitani, Saori Yada, Aya Sato, Eiichi Morii, Yoshihiro Shimizu, Hiroki R Ueda

    PLoS biology   23 ( 1 )   e3002707   2025.1

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

    Antibodies are extensively used in biomedical research, clinical fields, and disease treatment. However, to enhance the reproducibility and reliability of antibody-based experiments, it is crucial to have a detailed understanding of the antibody's target specificity and epitope. In this study, we developed a high-throughput and precise epitope analysis method, DECODE (Decoding Epitope Composition by Optimized-mRNA-display, Data analysis, and Expression sequencing). This method allowed identifying patterns of epitopes recognized by monoclonal or polyclonal antibodies at single amino acid resolution and predicted cross-reactivity against the entire protein database. By applying the obtained epitope information, it has become possible to develop a new 3D immunostaining method that increases the penetration of antibodies deep into tissues. Furthermore, to demonstrate the applicability of DECODE to more complex blood antibodies, we performed epitope analysis using serum antibodies from mice with experimental autoimmune encephalomyelitis (EAE). As a result, we were able to successfully identify an epitope that matched the sequence of the peptide inducing the disease model without relying on existing antigen information. These results demonstrate that DECODE can provide high-quality epitope information, improve the reproducibility of antibody-dependent experiments, diagnostics and therapeutics, and contribute to discover pathogenic epitopes from antibodies in the blood.

    DOI： 10.1371/journal.pbio.3002707

    PubMed

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  • Whole‐brain Cellome‐Wide Association Study (CWAS) Unveils Ultra‐Early Neurodegeneration Phenomena in a 3D Spatial Cell Atlas Reviewed

    Tomoki T Mitani, Kosei Yamaura, Katsuhiko Matsumoto, Rikuhiro Yamada, Etsuo A Susaki, Hiroki R Ueda

    Alzheimer's &amp; Dementia   20 ( S1 )   2024.12

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    Authorship：Lead author,　Corresponding author   Language：English   Publishing type：Research paper (scientific journal)   Publisher：Wiley  

    Abstract

    Background

    In aging societies, neurodegenerative diseases, such as Alzheimer’s disease, are receiving attention. These diseases are primary targets for preemptive medicine, emphasizing the importance of early detection and preventive treatment before the onset of severe, treatment‐resistant damages. However, there is a lack of comprehensive investigation of lesions and molecular targets in the entire organ, whereas spatial identification of early‐stage lesions is potentially overlooked at the single‐cell level.

    Method

    Here, we propose a novel approach, CWAS (whole body/organ cellome‐wide association studies), which integrates and analyzes spatio‐temporal cellular information across the entire mouse organ into a comprehensive organ cell atlas using tissue‐clearing imaging technologies [1,2].

    Result

    In our initial application to neurodegenerative models, we have been able to identify previously unreported neural degenerations at specific times and locations at the single‐cell level. In addition, our time‐series analysis in a mouse model of Alzheimer’s disease revealed the possible simultaneous onset of amyloid deposition and neurodegeneration, challenging the traditional amyloid hypothesis. Furthermore, we were able to identify unique multicellular inflammation networks surrounding neurodegenerative lesions in several disease models.

    Conclusion

    Our findings establish the concept of “spatial cellomics” realized through spatially precise organ mapping and integrated multiomics analysis at the single‐cell level. This approach shifts pathology, providing deeper insight into disease mechanisms and preventive strategies.

    References

    [1] Murakami TC, et al. Nat Neurosci. 2018;21(4):625‐637.

    [2] Matsumoto K*, Mitani TT*, Horiguchi SA, et al*. (*equal contribution) Nat Protoc. 2019;14(12):3506‐3537.

    DOI： 10.1002/alz.088470

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  • A novel tauopathy model mimicking molecular and spatial aspects of human tau pathology Reviewed

    Rin Yanai, Tomoki T Mitani, Etsuo A Susaki, Takeharu Minamihisamatsu, Masafumi Shimojo, Yuri Saito, Hiroshi Mizuma, Nobuhiro Nitta, Daita Kaneda, Yoshio Hashizume, Gen Matsumoto, Kentaro Tanemura, Ming-Rong Zhang, Makoto Higuchi, Hiroki R Ueda, Naruhiko Sahara

    Brain Communications   2024.9

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    Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)   Publisher：Oxford University Press (OUP)  

    Abstract

    Creating a mouse model that recapitulates human tau pathology is essential for developing strategies to intervene in tau-induced neurodegeneration. However, mimicking the pathological features seen in human pathology often involves a trade-off with artificial effects such as unexpected gene insertion and neurotoxicity from the expression system. To overcome these issues, we developed the rTKhomo mouse model by combining a transgenic CaMKII-tTA system with a P301L mutated 1N4R human tau knock-in at the Rosa26 locus with a C57BL/6J background. This model closely mimics human tau pathology, particularly in the hippocampal CA1 region, showing age-dependent tau accumulation, neuronal loss, and neuroinflammation. Notably, whole-brain 3D staining and light-sheet microscopy revealed a spatial gradient of tau deposition from the entorhinal cortex to the hippocampus, similar to the spatial distribution of Braak neurofibrillary tangle (NFT) staging. Furthermore, [18F]PM-PBB3 positron emission tomography (PET) imaging enabled the quantification and live monitoring of tau deposition. The rTKhomo mouse model shows potential as a promising next-generation preclinical tool for exploring the mechanisms of tauopathy and for developing interventions targeting the spatial progression of tau pathology.

    DOI： 10.1093/braincomms/fcae326

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  • Genome-wide epitope identification with single-amino-acid resolution via high-throughput and unbiased peptide analysis

    Katsuhiko Matsumoto, Shoko Y. Harada, Shota Y. Yoshida, Ryohei Narumi, Tomoki T. Mitani, Saori Yada, Aya Sato, Eiichi Morii, Yoshihiro Shimizu, Hiroki R. Ueda

    Preprint (bioRxiv)   2024.6

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    Publisher：Cold Spring Harbor Laboratory  

    Abstract

    Antibodies are extensively used in biomedical research, clinical fields, and disease treatment. However, to enhance the reproducibility and reliability of antibody-based experiments, it is crucial to have a detailed understanding of the antibody’s target specificity and epitope. In this study, we developed a high-throughput and precise epitope analysis method, DECODE (Decoding Epitope Composition by Optimized-mRNA-display, Data analysis, and Expression sequencing). This method allowed identifying patterns of epitopes recognized by monoclonal or polyclonal antibodies at single amino acid resolution and predicted cross-reactivity against the entire protein database. By applying the obtained epitope information, it has become possible to develop a new 3D immunostaining method that increases the penetration of antibodies deep into tissues. Furthermore, to demonstrated the applicability of DECODE to more complex blood antibodies, we performed epitope analysis using serum antibodies from mice with experimental autoimmune encephalomyelitis (EAE). As a result, we were able to successfully identify an epitope that matched the sequence of the peptide inducing the disease model without relying on existing antigen information. These results demonstrate that DECODE can provide high-quality epitope information, improve the reproducibility of antibody-dependent experiments, diagnostics and therapeutics, and contribute to discover pathogenic epitopes from antibodies in the blood.

    DOI： 10.1101/2024.06.13.598778

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  • Realization of cellomics to dive into the whole-body or whole-organ cell cloud. Reviewed International journal

    Tomoki T Mitani, Etsuo A Susaki, Katsuhiko Matsumoto, Hiroki R Ueda

    Nature methods   2024.6

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

    DOI： 10.1038/s41592-024-02307-5

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  • WHOLE-BRAIN CELLOME-WIDE ASSOCIATION STUDY (CWAS) UNVEILS NEURODEGENERATIVE TRAJECTORIES IN A 3D CELLULAR LANDSCAPE Reviewed

    Tomoki T Mitani, Katsuhiko Matsumoto, Hiroki R Ueda

    IBRO Neuroscience Reports   15 ( 1 )   S451 - S451   2023.10

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    Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)   Publisher：Elsevier BV  

    DOI： 10.1016/j.ibneur.2023.08.873

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  • Distinct phosphorylation states of mammalian CaMKIIβ control the induction and maintenance of sleep Reviewed

    Daisuke Tone, Koji L. Ode, Qianhui Zhang, Hiroshi Fujishima, Rikuhiro G. Yamada, Yoshiki Nagashima, Katsuhiko Matsumoto, Zhiqing Wen, Shota Y. Yoshida, Tomoki T. Mitani, Yuki Arisato, Rei-ichiro Ohno, Maki Ukai-Tadenuma, Junko Yoshida Garçon, Mari Kaneko, Shoi Shi, Hideki Ukai, Kazunari Miyamichi, Takashi Okada, Kenta Sumiyama, Hiroshi Kiyonari, Hiroki R. Ueda

    PLOS Biology   20 ( 10 )   e3001813 - e3001813   2022.10

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    Publishing type：Research paper (scientific journal)   Publisher：Public Library of Science (PLoS)  

    The reduced sleep duration previously observed in Camk2b knockout mice revealed a role for Ca<sup>2+</sup>/calmodulin-dependent protein kinase II (CaMKII)β as a sleep-promoting kinase. However, the underlying mechanism by which CaMKIIβ supports sleep regulation is largely unknown. Here, we demonstrate that activation or inhibition of CaMKIIβ can increase or decrease sleep duration in mice by almost 2-fold, supporting the role of CaMKIIβ as a core sleep regulator in mammals. Importantly, we show that this sleep regulation depends on the kinase activity of CaMKIIβ. A CaMKIIβ mutant mimicking the constitutive-active (auto)phosphorylation state promotes the transition from awake state to sleep state, while mutants mimicking subsequent multisite (auto)phosphorylation states suppress the transition from sleep state to awake state. These results suggest that the phosphorylation states of CaMKIIβ differently control sleep induction and maintenance processes, leading us to propose a “phosphorylation hypothesis of sleep” for the molecular control of sleep in mammals.

    DOI： 10.1371/journal.pbio.3001813

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  • A novel three-dimensional imaging system based on polysaccharide staining for accurate histopathological diagnosis of inflammatory bowel diseases. Reviewed International journal

    Satoshi Nojima, Shoichi Ishida, Kei Terayama, Katsuhiko Matsumoto, Takahiro Matsui, Shinichiro Tahara, Kenji Ohshima, Hiroki Kiyokawa, Kansuke Kido, Koto Ukon, Shota Y Yoshida, Tomoki T Mitani, Yuichiro Doki, Tsunekazu Mizushima, Yasushi Okuno, Etsuo A Susaki, Hiroki R Ueda, Eiichi Morii

    Cellular and molecular gastroenterology and hepatology   14 ( 4 )   905 - 924   2022.7

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

    BACKGROUND & AIMS: Tissue-clearing and three-dimensional (3D) imaging techniques aid clinical histopathological evaluation; however, further methodological developments are required prior to use in clinical practice. METHODS: We sought to develop a novel fluorescence staining method based on the classical PAS stain. We further attempted to develop a 3D imaging system based on this staining method and evaluated whether the system can be employed for quantitative 3D pathological evaluation and deep learning-based automatic diagnosis of inflammatory bowel diseases. RESULTS: We successfully developed a novel periodic acid-FAM hydrazide (PAFhy) staining method for 3D imaging when combined with a tissue-clearing technique (PAFhy-3D). This strategy enabled clear and detailed imaging of the 3D architectures of crypts in human colorectal mucosa. PAFhy-3D imaging also revealed abnormal architectural changes in crypts in ulcerative colitis tissues and identified the distributions of neutrophils in cryptitis and crypt abscesses. PAFhy-3D revealed novel pathological findings including "spiral staircase-like crypts" specific to inflammatory bowel diseases. Quantitative analysis of crypts based on 3D morphological changes enabled differential diagnosis of ulcerative colitis, Crohn's disease, and non-inflammatory bowel disease; such discrimination could not be achieved by pathologists. Furthermore, a deep learning-based system employing PAFhy-3D images was used to distinguish these diseases The accuracies were excellent (macro-average AUC = 0.94; F1 scores = 0.875 for ulcerative colitis, 0.717 for Crohn's disease, and 0.819 for non-inflammatory bowel disease). CONCLUSIONS: PAFhy staining and PAFhy-3D imaging are promising approaches for next-generation experimental and clinical histopathology.

    DOI： 10.1016/j.jcmgh.2022.07.001

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  • Realization of phosphorylation hypothesis of sleep by mammalian CaMKIIβ

    Daisuke Tone, Koji L. Ode, Qianhui Zhang, Hiroshi Fujishima, Rikuhiro G. Yamada, Yoshiki Nagashima, Katsuhiko Matsumoto, Zhiqing Wen, Shota Y. Yoshida, Tomoki T. Mitani, Rei-ichiro Ohno, Maki Ukai-Tadenuma, Junko Yoshida Garçon, Mari Kaneko, Shoi Shi, Hideki Ukai, Kazunari Miyamichi, Takashi Okada, Kenta Sumiyama, Hiroshi Kiyonari, Hiroki R. Ueda

    Preprint (bioRxiv)   2021.10

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    Publisher：Cold Spring Harbor Laboratory  

    ABSTRACT

    The reduced sleep duration observed in Camk2a and Camk2b knockout mice revealed the role of Ca<sup>2+</sup>/calmodulin-dependent protein kinase II (CaMKII)α/CAMKIIβ as sleep-promoting kinases and lead to the phosphorylation hypothesis of sleep. However, the underlying mechanism of sleep regulation by kinases and protein phosphorylation is largely unknown. Here, we demonstrate that the phosphorylation states of CaMKIIβ regulates sleep duration and sleep needs. Importantly, the activation or inhibition of CaMKIIβ can increase or decrease sleep duration by almost two-fold, supporting the role of CaMKIIβ as a core sleep regulator in mammals. This sleep regulation depends on the kinase activity of CaMKIIβ in excitatory neurons. Furthermore, CaMKIIβ mutants mimicking different phosphorylation states can regulate various sleep steps including sleep induction, sleep maintenance, and sleep cancelation. Key CaMKIIβ residues responsible for the mode switch undergo ordered (auto-)phosphorylation. We thus propose that ordered multi-site phosphorylation of CaMKIIβ underlies multi-step sleep regulation in mammals.

    DOI： 10.1101/2021.10.11.463945

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  • Amyotrophic lateral sclerosis with speech apraxia, predominant upper motor neuron signs, and prominent iron accumulation in the frontal operculum and precentral gyrus. Reviewed International journal

    Tomoki T Mitani, Goichi Beck, Kansuke Kido, Rika Yamashita, Yuki Yonenobu, Takuya Ogawa, Chizu Saeki, Tatsusada Okuno, Seiichi Nagano, Eiichi Morii, Masato Hasegawa, Yuko Saito, Shigeo Murayama, Hideki Mochizuki

    Neuropathology : official journal of the Japanese Society of Neuropathology   41 ( 4 )   324 - 331   2021.8

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    Authorship：Lead author   Language：English  

    Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease; transactivation response DNA-binding protein of 43 kDa (TDP-43) and iron accumulation are supposed to play a crucial role in the pathomechanism of the disease. Here, we report an unusual case of a patient with ALS who presented with speech apraxia as an initial symptom and upper motor neuron deficiencies. In the early clinical stages, single-photon emission computed tomography visualized focal hypoperfusion of the right frontal operculum, and magnetic resonance imaging identified a hypointense area along the frontal lobe on T2-weighted images. Neuropathological examination revealed that neuronophagia of Betz cells, gliosis, appearance of phosphorylated TDP-43 (p-TDP-43)-positive glial and neuronal inclusions, and prominent iron accumulation were frequently visible in the precentral gyrus. TDP-43 pathology and focal iron accumulation were also visible in the frontal operculum, but only a mild neuronal loss and a few p-TDP-43-positive neuronal and glial inclusions were found in the hypoglossal nucleus of the medulla oblongata and anterior horn of the spinal cord. Immunoblot analysis revealed an atypical band pattern for ALS. In our case, abnormal TDP-43 and iron accumulation might possibly have caused neurodegeneration of the frontal operculum, in tandem or independently; it might then have spread into the primary motor area. Our results suggest a causative association between TDP-43 and iron accumulation in the pathomechanisms of ALS presenting with upper motor neuron signs.

    DOI： 10.1111/neup.12763

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  • Advanced CUBIC tissue clearing for whole-organ cell profiling Reviewed

    Katsuhiko Matsumoto, Tomoki T. Mitani, Shuhei A. Horiguchi, Junichi Kaneshiro, Tatsuya C. Murakami, Tomoyuki Mano, Hiroshi Fujishima, Ayumu Konno, Tomonobu M. Watanabe, Hirokazu Hirai, Hiroki R. Ueda

    Nature Protocols   14 ( 12 )   3506 - 3537   2019.12

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

    DOI： 10.1038/s41596-019-0240-9

    Web of Science

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    Other Link： http://www.nature.com/articles/s41596-019-0240-9

  • A report for International medical care of Zambia Reviewed

    Tomoki T. Mitani, Yasuhide Nakamura

    Journal of international society of clinical medicine   1 ( 1 )   33 - 34   2017.12

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

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Books

  • Next-generation whole-organ all-cell imaging driven by MOVIE microscopy

    Tomoki T. Mitani, Katsuhiko Matsumoto, Hiroki R. Ueda（ Role： Contributor）

    2023.12 

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  • 3D pathology by tissue-clearing technique

    Katsuhiko Matsumoto, Tomoki T. Mitani, Hiroki R. Ueda（ Role： Joint author）

    Precision Medicine  2023.7 

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  • Whole-organ cells profiling using tissue-clearing method "CUBIC"

    Tomoki T. Mitani, Matsumoto Katsuhiko, Hiroki R. Ueda（ Role： Joint author ,  1-4）

    Precision Medicine  2019.1 

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MISC

  • 神経変性疾患関連因子の睡眠表現型スクリーニングによる新規睡眠覚醒制御因子の同定

    山浦港生, 山浦港生, 戸根大輔, 山田陸裕, 三谷智樹, 三谷智樹, 上田泰己, 上田泰己, 上田泰己

    日本神経化学会大会抄録集(Web)   65th   2022

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Presentations

  • Whole-Brain Single-Neuron Atlas-driven 3D Pathology Reveals Microglial Security Hole Accelerating Neuronal Vulnerability Invited

    Tomoki T Mitani

    The 23rd Annual Meeting of Japanese Society of Digital Pathology in 2025  2025.9 

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    Event date： 2025.9

    Language：English   Presentation type：Oral presentation (general)  

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  • Whole-Brain Single-Neuron Atlas Analysis Reveals Microglial Security Hole Accelerating Neuronal Vulnerability Invited

    Tomoki T. Mitani

    The 68th Annual Meeting of the Japanese Society for Neurochemistry (JSN)  2025.9 

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    Event date： 2025.9

    Language：English   Presentation type：Symposium, workshop panel (public)  

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  • Whole-Brain Single-Neuron Atlas Uncovers Microglial Security Hole Accelerating Neuronal Vulnerability

    Tomoki T. Mitani

    The 48th Annual Meeting of the Japan Neuroscience Society  2025.7 

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    Event date： 2025.7

    Language：English   Presentation type：Poster presentation  

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  • Whole-Brain Single-Neuron Atlas Uncovers Microglial Security Hole Accelerating Neuronal Vulnerability

    Tomoki T. Mitani

    The 48th Annual Meeting of the Japan Neuroscience Society (The International Exchange Meeting for Young Researchers)  2025.7 

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    Event date： 2025.7

    Language：English   Presentation type：Poster presentation  

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  • The “Developmental Biology” of Whole-Brain Neurodegenerative Pathology Based on Time-Series Light-Sheet Microscopy Imaging Invited

    Tomoki T. Mitani

    Joint Meeting of JSCB 77th and JSDB 58th  2025.7 

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    Event date： 2025.7

    Language：Japanese   Presentation type：Symposium, workshop panel (public)  

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  • The “Developmental Biology” of Whole-Brain Neurodegenerative Pathology Based on Time-Series Light-Sheet Microscopy Imaging (Best Presentation Award for Young Scientists) Invited

    Tomoki T. Mitani

    Joint Meeting of JSCB 77th and JSDB 58th  2025.7 

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    Event date： 2025.7

    Language：English   Presentation type：Oral presentation (invited, special)  

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  • Whole-Brain Cellome-Wide Association Study (CWAS) reveals Microscale Neurodegenerative Trajectories in a 3D Cellular Landscape

    Tomoki T Mitani, Kosei Yamaura, Katsuhiko Matsumoto, Etsuo A. Susaki, Hiroki R. Ueda

    The 46th Annual Meeting of the Molecular Biology Society of Japan  2023.12 

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    Event date： 2023.12

    Language：English   Presentation type：Poster presentation  

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  • Whole-brain Cellome-Wide Association Study (CWAS) reveals neurodegenerative trajectories in a 3D cellular landscape

    T. T. MITANI, K. YAMAURA, K. MATSUMOTO, E. A. SUSAKI, H. R. UEDA

    Neuroscience 2023  2023.11 

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    Event date： 2023.11

    Language：English   Presentation type：Poster presentation  

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  • WHOLE-BRAIN CELLOME-WIDE ASSOCIATION STUDY (CWAS) UNVEILS NEURODEGENERATIVE TRAJECTORIES IN A 3D CELLULAR LANDSCAPE

    Tomoki T Mitani, Katsuhiko Matsumoto, Hiroki R Ueda

    the 11th IBRO World Congress of Neuroscience  2023.9 

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    Event date： 2023.9

    Language：English   Presentation type：Poster presentation  

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  • Whole-brain imaging of all neurons in mice.

    Tomoki T. Mitani, Katsuhiko Matsumoto, Hiroki R. Ueda

    The 14th "Hikari-Juku" (Young Researchers' Meeting on Light Imaging)  2023.1 

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    Event date： 2023.1

    Language：English   Presentation type：Poster presentation  

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  • Whole-brain neuron profiling identifies biological alterations in three-dimensional structure and function at a single-neuron level

    T. T. MITANI, S. Y. YOSHIDA, K. YAMAURA, K. MATSUMOTO, E. A. SUSAKI, H. R. UEDA

    Neuroscience 2022  2022.11 

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    Event date： 2022.11

    Language：English   Presentation type：Poster presentation  

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  • Cellomics accelerated by cleared organs with an application for neurology

    Tomoki T. Mitani, Katsuhiko Matsumoto, Hiroki R.Ueda

    Neuro2022  2022.6 

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    Event date： 2022.6 - 2022.7

    Language：English   Presentation type：Oral presentation (general)  

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  • Cleared Brain Driven Cellomics Invited

    Tomoki T. Mitani

    63rd Annual Meeting of the Japanese Society of Neurology  2022.5 

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    Event date： 2022.5

    Language：Japanese   Presentation type：Symposium, workshop panel (nominated)  

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  • Whole-organ cell profiling at single-cell level combined with CUBIC tissue clearing

    Tomoki T. Mitani, Katsuhiko Matsumoto, Shuhei A. Horiguchi, Hiroki R. Ueda

    The 2th Annual Meeting of the Quantum Life Science Society  2020.12 

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    Event date： 2020.12

    Language：Japanese   Presentation type：Poster presentation  

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  • High-speed, high-resolution light-sheet microscopy for Cellomics of neurodegenerative diseases Invited

    Tomoki T. Mitani

    Invited Seminar, School of Medicine, Osaka Metropolitan University  2025.10 

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  • High-speed, high-resolution light-sheet microscopy for Cellomics of neurodegenerative diseases Invited

    Tomoki T. Mitani

    Invited Seminar, Keio University School of Medicine  2025.10 

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  • High-Resolution, High-Speed Light-Sheet Microscopy for Whole-Organ Cell Profiling in Neurological Diseases Invited

    Tomoki T Mitani

    66th Annual Meeting of the Japanese Society of Neurology  2025.5 

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    Language：Japanese   Presentation type：Symposium, workshop panel (nominated)  

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  • Whole Brain Single Neuron Atlas Uncovers a Novel Neurodegenerative Niche, “Microglia Security Hole” Invited

    Tomoki T Mitani

    66th Annual Meeting of the Japanese Society of Neurology  2025.5 

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    Language：English   Presentation type：Symposium, workshop panel (nominated)  

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  • Whole-Brain Cellular Decoding of Neurodegenerative Lesions Using Longitudinal Whole-Brain Light-Sheet Microscopy Imaging Invited

    Tomoki T. Mitani

    Niigata Brain and Nerve Research Society Special Meeting  2025.4 

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    Presentation type：Oral presentation (invited, special)  

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  • Whole-brain Cellome-Wide Association Study (CWAS) Unveils Ultra-Early Neurodegeneration Phenomena in a 3D Spatial Cell Atlas

    Tomoki T Mitani, Kosei Yamaura, Katsuhiko Matsumoto, Rikuhiro Yamada, Etsuo A Susaki, Hiroki R Ueda

    2024.7 

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    Language：English   Presentation type：Poster presentation  

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  • Whole-brain Cellome-Wide Association Study (CWAS) Unveils Ultra-Early Neurodegeneration Phenomena in a 3D Spatial Cell Atlas

    Tomoki T Mitani, Kosei Yamaura, Katsuhiko Matsumoto, Rikuhiro Yamada, Etsuo A Susaki, Hiroki R Ueda

    Alzheimer’s Imaging Consortium (AIC) Preconference  2024.7 

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    Language：English   Presentation type：Poster presentation  

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  • Whole-Brain Cellome-Wide Association Study (CWAS) reveals Microscale Neurodegenerative Trajectories in a 3D Cellular Landscape Invited

    Tomoki T. Mitani

    National Institutes for Quantum Science and Technology (QST)  2024.2 

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    Language：Japanese   Presentation type：Public lecture, seminar, tutorial, course, or other speech  

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  • Cellome-Wide Association Studies (CWAS) for Comprehensive 3D Analysis of Spatial Lesions and Microenvironments Invited

    Tomoki T Mitani

    An invitation-only seminar hosted by Beth Israel Deaconess Medical Center/Harvard Medical School  2023.11 

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    Language：English   Presentation type：Public lecture, seminar, tutorial, course, or other speech  

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  • Towards Single-Cell Precision Medicine: Ultra-Early Detection in Neurodegeneration with 3D Subcellular Light-Sheet Imaging Invited

    Tomoki T Mitani

    An invitation-only seminar hosted by the Interdisciplinary Brain Center (IBC) and the Alzheimer's Clinical & Translational Research Unit (ACTRU) at Massachusetts General Hospital, affiliated with Harvard Medical School, located in Boston, MA.  2023.11 

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    Language：English   Presentation type：Public lecture, seminar, tutorial, course, or other speech  

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  • Whole-brain Cellome-Wide Association Study (CWAS) reveals ultra-early neurodegenerative niches at single-cell resolution

    Tomoki T Mitani

    BDR student symposium 2023  2023.6 

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    Language：English   Presentation type：Poster presentation  

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  • Cellomics-neurology at whole-brain scale for biomedical research

    Tomoki T. Mitani

    BDR Student Symposium 2021  2021.5 

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    Language：English   Presentation type：Oral presentation (general)  

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  • Cellomics-neurology by CUBIC, 3D immunostaining and high-speed imaging at whole-brain scale

    Tomoki Mitani

    62nd Annual Meeting of the Japanese Society of Neurology  2021.5 

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    Language：English   Presentation type：Oral presentation (general)  

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  • Advanced CUBIC pipeline in whole-organ cell profiling for biomedical research International conference

    Tomoki T. Mitani, Katsuhiko Matsumoto, Shuhei A Horiguchi, Junichi Kaneshiro, Tatsuya C Murakami, Tomoyuki Mano, Hiroshi Fujishima, Ayumu Konno, Tomonobu M Watanabe, Hirokazu Hirai, Hiroki R Ueda

    Society for Neuroscience 2019 annual meeting  2019.10 

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  • 次世代イメージングで切り開く全臓器における全細胞プロファイリング Invited

    三谷 智樹

    国立がん研究センター 招待セミナー  2019.9 

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    Language：Japanese   Presentation type：Oral presentation (invited, special)  

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  • Whole-organ cell profiling accelerated by CUBIC combined with MOVIE imaging, International conference

    Tomoki T. Mitani, Katsuhiko Matsumoto, Shuhei A Horiguchi, Junichi Kaneshiro, Tatsuya C Murakami, Tomoyuki Mano, Hiroshi Fujishima, Ayumu Konno, Tomonobu M, Watanabe, Hirokazu Hirai, Hiroki R Ueda

    The 6th International Symposium on Bioimaging  2019.9 

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  • Whole-organ cell profiling accelerated by CUBIC combined with MOVIE imaging International conference

    Tomoki T. Mitani, Katsuhiko Matsumoto, Shuhei A Horiguchi, Junichi Kaneshiro, Tatsuya C Murakami, Tomoyuki Mano, Hiroshi Fujishima, Ayumu Konno, Tomonobu M Watanabe, Hirokazu Hirai, Hiroki R Ueda

    The 6th International Symposium on Bioimaging  2019.9 

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    Language：English   Presentation type：Oral presentation (invited, special)  

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  • A case report for international medicine of Zambia

    Tomoki T. Mitani, Yasuhide Nakamura

    2016.12 

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    Language：Japanese   Presentation type：Oral presentation (general)  

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Industrial property rights

  • 特願2021-052469 走査型蛍光顕微鏡

    三谷 智樹, 松本 桂彦, 上田 泰己

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    Applicant：株式会社ＣＵＢＩＣＳｔａｒｓ

    Application no：特願2021-052469  Date applied：2022.7

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  • MICROSCOPE, VIEWING METHOD, CONTROL PROGRAM AND DEVICE

    Tomoki T. Mitani, Katsuhiko Matsumoto, Hiroki R. Ueda

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    Application no：特願2019-137924  Date applied：2019.7

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Awards

  • Best Presentation Award

    2025.9   Japanese Society for Neurochemistry  

    Tomoki T. Mitani

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  • Best Presentation Award for Young Scientists

    2025.7   Japan Society for Cell Biology  

    Tomoki T. Mitani

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  • Study aboroad Grants

    2024.12   Japan Research Foundation for Clinical Pharmacology  

    Tomoki T. Mitani

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  • Best Poster Presentation Award (PI Choice Award)

    2023.6   RIKEN BDR Student Symposium 2023  

    Tomoki T. Mitani

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  • Takeda Science Foundation Award for Outstanding Research Achievement in Medical School Doctoral Program

    2023.5  

    Tomoki T. Mitani

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  • Takeda Science Foundation Scholarship for Medical School Doctoral Program

    2021.5  

    Tomoki T. Mitani

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  • The Best Imaging Award "Carl Zeiss Award"

    2019.9   The 6th International Symposium on Bioimaging  

    Mitani T. Tomoki

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Research Projects

  • Establishment of a Large-Scale Cellomics Platform for Elucidating Early Neurodegeneration in the Human Brain

    Grant number：25wm0625129h0001

    2025.8 - 2028.3

    Awarding organization：Japan Agency for Medical Research and Development（AMED）

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    Authorship：Principal investigator 

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  • 早期神経変性病巣を対象とした全脳マルチセルオミクス法の確立

    Grant number：25K10180

    2025.4 - 2028.3

    System name：科学研究費助成事業

    Research category：基盤研究(C)

    Awarding organization：日本学術振興会

    三谷 智樹

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    Grant amount：\4550000 （ Direct Cost: \3500000 、 Indirect Cost：\1050000 ）

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  • CWAS Analysis to Profile Comprehensive Neurodegenerative Lesions Towards Integrated Omics

    2024.10 - 2027.3

    System name：Life phenomena and functional materials

    Awarding organization：Japan Science and Technology Agency, National Research and Development Agency

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    Authorship：Principal investigator 

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  • 全脳ニューロンアトラスによる神経変性疾患モデルの一細胞解像度全脳病態解析

    Grant number：20K16498

    2020.4 - 2023.3

    System name：科学研究費助成事業

    Research category：若手研究

    Awarding organization：日本学術振興会

    三谷 智樹

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    Grant amount：\4290000 （ Direct Cost: \3300000 、 Indirect Cost：\990000 ）

    これまでの神経変性疾患研究は、異常タンパク質の蓄積を代表とする神経細胞内毒性の分子機構、さらに近年ではグリア細胞も含めた脳内環境の重要性を解明してきたが、病態解明はごく一部の典型的部位に制限されており、未知の病変が数多く残っている。例えば、パーキンソン病において認知機能低下や鬱症状、幻覚、レム睡眠行動異常症(延髄)、注意障害(前頭葉)といった非運動症状が最近注目されているが、病態解明にはごく一部(中脳-黒質-線条体)しか解析されておらず、脳全体を俯瞰的に見て何がどこでどのような順で起きているのかは全くわかっていない。その詳細を明らかにするためには、全脳の細胞情報を一細胞レベルで網羅的に調べ上げる必要があるが、これまでにそのような報告はない。
    本研究課題では、研究代表者により構築した成体マウス脳の全細胞解析と3次元組織学的染色法を組み合わせることで、神経変性疾患の全脳病態研究の基盤を構築することを確立することを目的とする。
    本研究課題開始時より、全脳の免疫染色と全自動神経検出を実証してきており、実際に神経変性モデルに応用を行った。しかしながら小脳や海馬など細胞密度の高い場所での神経細胞検出の感度が低いことが課題となり、今年度は正確な細胞検出に向けて、1) 高Z分解能の顕微鏡の開発、2) 高精度細胞検出解析法の開発に取り組んだ。1,2ともに開発はおおむねうまくいっており、マウス全脳の小脳・海馬を含んだあらゆる領域でF-score 0.9を超える高精度な神経細胞検出を成功させることができた。また本手法をミクログリアマーカーに対して行うことにも成功しているため、ミクログリアの解析を通じて神経変性疾患の病態研究において炎症病態の解明が期待できる。本年度は、複数の神経変性モデルでこの高精細な技術で一細胞レベルでの神経変性の解析を行うことでパイプラインを実証し、論文投稿を予定している。

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Media Coverage

  • Developing high-speed imaging and analysis technologies to investigate all cells within an organ Internet

    Yahoo News  2020.1

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  • Developing high-speed imaging and analysis technologies to investigate all cells within an organ Internet

    MONOist  2020.1

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    Author：Other 

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  • Developing high-speed imaging and analysis technologies to investigate all cells within an organ Internet

    NewsPicks  2020.1

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