Details of the Researcher

PHOTO

Ami Kobayashi
Section
Institute of Medical Research
Job title
Senior Assistant Professor
Degree
  • PhD (The University of Tokyo)

  • MD

Professional Memberships 9

  • 日本医学教育学会

  • International Society for Neurochemistry (ISN)

  • 日本認知症学会

  • 日本内科学会

  • 日本老年医学会

  • 日本神経化学会

  • 日本神経科学学会

  • 日本神経学会

  • 日本基礎老化学会

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Research Areas 2

  • Life sciences / Neurology /

  • Life sciences / Neuroscience - general /

Awards 11

  1. Young Investigator Colloquiums (YIC)

    2026/08 Asian-Pacific Society for Neurochemistry ISN-APSN-Young Investigators Colloquium

  2. The 5th Marie Sklodowska Curie Award

    2026/06 Japan Science and Technology Agency

  3. JSPS Overseas Research Fellowships

    2025/01 Japan Society for the Promotion of Science

  4. The Uehara Memorial Foundation Fellowship Award

    2024/01 The Uehara Memorial Foundation

  5. Young Member's Symposia Award, International Society for Neurochemistry (ISN) 2023 meeting

    2023/08 International Society for Neurochemistry (ISN)

  6. 第66回日本神経化学会大会 鍋島トラベルアワード

    2023/07 日本神経化学学会

  7. 第66回日本神経化学会大会 若手道場優秀発表賞

    2023/07 日本神経化学学会

  8. Travel Fellowship Award, Tau Consortium Investigator's Meeting 2023

    2023/06

  9. 第41回日本認知症学会学術集会/第37回日本老年精神医学会 合同奨励賞(基礎部門)

    2022/11 日本認知症学会

  10. 第44回日本基礎老化学会大会 若手奨励賞

    2021/06 日本基礎老化学会

  11. 第44回日本基礎老化学会大会 Most Impressive Presentator賞

    2021/06 FRET-based high-throughput screen identifies a compound that promotes mitochondrial function by respiratory chain supercomplex assembly

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Papers 25

  1. Augmenting Radiation Sensitivity by Targeting PAR-Dependent Replication Fork Vulnerability in IDH-Mutant Glioma Peer-reviewed

    Yosuke Kitagawa, Ali Nasser, Ami Kobayashi, Ethan Wetzel, Lisa Melamed, Chia-Chen Chang, Hiroaki Nagashima, Julie J. Miller, Hiroaki Wakimoto, Daniel P. Cahill

    bioRxiv : the preprint server for biology 2026/08/10

    DOI: 10.64898/2026.08.08.743634  

  2. Simulating interprofessional collaboration: An asynchronous online activity Peer-reviewed

    Ami Kobayashi, Julianna Lau, Blaire Rikard, Yulia Murray, Jennifer Prisco, Jennifer Kesselheim, Kelsey Miller

    Medical Education 2026/08

    DOI: 10.1111/medu.70175  

  3. tRNA-derived fragments are elevated in the aging brain and may contribute to neurodegeneration International-journal

    Lien D. Nguyen, Ami Kobayashi, Alain Ndayisaba, Vikram Khurana, Pavel Ivanov, Anna M. Krichevsky

    bioRxiv : the preprint server for biology 2026/05/19

    DOI: 10.64898/2026.05.15.725455  

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    tRNA-derived fragments (tRFs) are a class of small noncoding RNAs with emerging roles in stress responses and gene regulation, yet their dynamics across tissues and brain regions during aging remain poorly understood. Here, we systematically profiled age-associated changes in tRFs using three independent mouse small RNA-seq datasets spanning multiple organs and brain regions. Nuclear-encoded tRFs were the only small RNA class showing a strong, progressive accumulation with age, a pattern that was specific to the brain and broadly distributed across brain regions. Fragment length distributions, boundary profiles, and coverage maps were consistent with amplified cleavage at conserved sites, implicating angiogenin as a primary driver. Age-associated increases in specific tRF species, including 5'Cys GCA , 5'Glu CTC , and 5'Gly GCC , were validated by northern blotting and RT-qPCR. Analogous upregulation was observed in human frontal lobe tissue from frontotemporal dementia patients and in cerebrospinal fluid from traumatic brain injury patients, suggesting that tRF accumulation is further amplified under neurological stress. Together, these findings establish nuclear-encoded tRFs as a small RNA class that accumulates selectively in the aging brain, with potential roles in neurodegeneration, and as biomarkers and targets for therapeutic intervention.

  4. tRNA-derived fragments elevated in Alzheimer’s disease facilitate Tau aggregation International-journal

    Ami Kobayashi, Prakash Kharel, Yanhong Zhang, Lien Nguyen, Maria Inmaculada Barrasa, Allison M. Williams, Vikram Khurana, Pavel Ivanov, Anna M. Krichevsky

    bioRxiv : the preprint server for biology 2026/05/18

    DOI: 10.64898/2026.05.17.725757  

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    UNLABELLED: Tauopathies, including Alzheimer's disease (AD), are driven by pathological Tau aggregation, a process that requires co-factors. Small RNAs (sRNA) have been proposed as such co-factors, yet little is known about endogenous transcripts that promote Tau pathology. We identify stress-induced tRNA-derived RNAs or fragments (tDRs/tRFs) as the most dysregulated sRNA class in human AD brains, PS19 mice overexpressing mutant human Tau, and human neuronal tauopathy models. Notably, the highly accumulating 5'Glu CTC and 5'Gly GCC tRFs induce Tau S396 phosphorylation, oligomerization, and impact neurite growth. Moreover, 5'Glu CTC is enriched in pathological Tau precipitates and co-localizes with oligomeric Tau in PS19 mouse brains. Inhibiting 5'Glu CTC mitigates Tau pathology. Furthermore, these tRFs are highly secreted by stressed neurons and can be taken up by recipient cells, implicating them in the propagation of pathology. Our findings establish 5'Glu CTC as a key regulator of Tau aggregation and suggest its inhibition as a promising therapeutic strategy for tauopathies. HIGHLIGHTS: Specific stress-induced 5'tRFs strongly accumulate in Alzheimer's disease brains 5'Glu CTC binds and co-localizes to pathologic Tau in neurons and in the brain 5'Glu CTC promotes Tau pathology while its inhibition reverses these effects Specific 5'tRFs are horizontally transferred between neurons.

  5. Comparison of Fluorescent Probes for IDH-Wildtype Glioblastoma, Metastatic Brain Tumors, and PCNSL: A Biomechanical Perspective International-journal Invited Peer-reviewed

    Zelong Zheng, Ami Kobayashi, Yosuke Kitagawa

    International Journal of Molecular Sciences 27 (10) 2026/05/17

    DOI: 10.3390/ijms27104495  

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    Intraoperative fluorescence-guided surgery is an important adjunct to brain tumor resection. However, fluorescent probe performance varies across molecularly and histopathologically distinct entities, including IDH-wildtype glioblastoma, metastatic brain tumors (MBTs), and primary central nervous system lymphoma (PCNSL), and the mechanisms underlying this variability remain poorly understood. We propose a mechanistic framework integrating biomechanical constraints, molecular barrier heterogeneity, and probe-specific pharmacokinetics to explain cross-tumor differences in fluorescence signal. Probe performance is conceptualized through three sequential bottlenecks: extravasation (blood-brain barrier/blood-tumor barrier permeability and transcytosis), interstitial penetration (extracellular matrix density and hydraulic resistance), and retention/clearance (efflux transporters and metabolic processing). An overlying optical layer, including tissue absorption, scattering, and autofluorescence, further modulates the detected signal. Tumor-specific molecular heterogeneity critically shapes these processes. In IDH-wildtype glioblastoma and legacy high-grade glioma cohorts, heterogeneous expression of ATP-binding cassette transporters has been associated with reduced intracellular accumulation of protoporphyrin IX after 5-aminolevulinic acid administration and may contribute to false-negative fluorescence in selected tumor regions. In MBTs, stage-dependent blood-tumor barrier integrity and vascular programs influence probe delivery, whereas in PCNSL, corticosteroid-sensitive restoration of endothelial barrier function may compromise the performance of leakage-dependent tracers. Together, this framework highlights how tumor biology, barrier function, and probe pharmacology jointly shape fluorescence contrast. Rational probe selection informed by tumor-specific transport and barrier constraints may improve intraoperative visualization of brain tumors and optimize surgical decision-making.

  6. Effects of Short- and Long-Term Mutant IDH1 Inhibition on Radiosensitivity Across Genetically Diverse Patient-derived IDH1-Mutant Glioma Cells Peer-reviewed

    Yosuke Kitagawa, Logan D Muzyka, Ami Kobayashi, Ethan Wetzel, Ali Nasser, Julie J Miller, Hiroaki Wakimoto, Daniel P Cahill

    Neuro-Oncology Advances 2026/03/02

    Publisher: Oxford University Press (OUP)

    DOI: 10.1093/noajnl/vdag057  

    eISSN: 2632-2498

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    Abstract Background IDH mutant gliomas produce the oncometabolite 2-hydroxyglutarate (2-HG), driving tumorigenesis through metabolic dysregulation and epigenetic alterations. IDH inhibitors (IDHi) reduce 2-HG and are clinically approved for treating IDH mutant gliomas. However, the observed impact of IDHi therapy on tumor response to ionizing radiation (IR) has been variable across murine models and engineered cell lines. Methods We investigated the effects of short-term (5 days) and long-term (≥5 weeks) exposure to the IDH1 inhibitor AGI-5198 on radiation-induced cytotoxicity. Patient-derived glioma neurosphere lines (MGG119, TS603S2, BT142, MGG152) were studied, with IDH1-mutant fibrosarcoma HT1080 and an inducible IDH1-R132H glioma line (MGG18 Tet±). Intracellular 2-HG, cell viability, and clonogenic survival were measured following IR. Results AGI-5198 potently reduced intracellular 2-HG across all IDH1-mutant lines after short-term treatment, with suppression maintained during prolonged exposure but rapidly reversed upon withdrawal. Long-term AGI exposure produced cell viability responses to both standard- and high-dose IR comparable to short-term treatment in HT1080, TS603S2, BT142, MGG152, and MGG18 Tet±. Across endogenous IDH-mutant models, neither short- nor long-term IDH inhibition induced radioresistance. MGG119, harboring IDH1-R132H and MET alterations, showed intrinsic radioresistance unaffected by IDHi. In contrast, MGG152, harboring IDH1-R132H and BRCA2 mutations, exhibited modest radiosensitization with IDHi. Conclusions Prolonged AGI-5198 exposure does not reduce IR sensitivity in IDH mutant glioma cells. Effects were comparable to short-term treatment, while radiation responses varied by genetic context. No deleterious interaction between IDHi and IR was observed in endogenous IDH-mutant cells except for MGG18 Tet+ supporting integration of IDHi with radiotherapy in IDH mutant gliomas.

  7. Development of Plasma Protein Classification Models for Alzheimer’s Disease Using Multiple Machine Learning Approaches Peer-reviewed

    Amy Tsurumi, Catherine M. Cahill, Andy J. Liu, Pranam Chatterjee, Sudeshna Das, Ami Kobayashi

    International Journal of Molecular Sciences 2025/12/02

    DOI: 10.3390/ijms262311673  

  8. Lipid nanoparticle formulation for gene editing and RNA-based therapies for glioblastoma. International-journal Peer-reviewed

    Yanhong Zhang, Rosalia Rabinovsky, Evgeny Deforzh, Ami Kobayashi, Anastasia Kuzkina, Johnna Francis Varghese, Damita Rai, Joanna A Korecka, Vikram Khurana, Gopal Murugaiyan, David Morrissey, Erik J Uhlmann, Anna M Krichevsky

    Neuro-oncology 2025/07/11

    DOI: 10.1093/neuonc/noaf162  

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    BACKGROUND: Glioblastoma (GBM), one of the deadliest cancers, resists current therapies, with drug development hindered by its high heterogeneity. However, GBM consistently relies on microRNA-10b (miR-10b), a key driver of glioma growth and a promising therapeutic target. miR-10b gene editing represents a potential treatment, but effective delivery strategies for gene editing systems in GBM remain unexplored. METHODS: We developed lipid nanoparticles (LNPs) encapsulating Cas9 mRNA and a miR-10b-targeting sgRNA (termed miRTEN). miRTEN was tested in glioma stem cells (GSCs) and orthotopic GBM models to assess therapeutic efficacy, immune responses, and safety. RESULTS: Intracerebroventricular (ICV) injections of miRTEN enabled broad and durable Cas9 mRNA expression and miR-10b gene editing in tumor core and invasive areas across diverse GBM models. miRTEN significantly suppressed tumor growth, reduced GSC proliferation and viability, with therapeutic outcomes correlating with dose-dependent miR-10b suppression. Combining miRTEN with temozolomide (TMZ) further enhanced tumor suppression, overcoming TMZ resistance and improving survival. In immunocompetent models, miRTEN activated anti-tumor immune responses, increased cytotoxic CD8+ T cells infiltration, and promoted durable immune memory, enabling tumor rejection upon rechallenge. Safety assessments demonstrated that miRTEN selectively targets GBM cells, sparing normal brain tissues and causing no significant off-target toxicity. CONCLUSION: As in vivo CRISPR-based drugs advance toward clinical applications, our findings demonstrate the potential of LNPs-mediated CRISPR-Cas9 systems for targeted miR-10b editing and, more generally, gene editing and RNA therapies for GBM. miRTEN monotherapy, as well as its combination with standard care, offers a promising, safe, and effective approach to improving outcomes in GBM.

  9. Novel Therapeutic Algorism in Patients With Anterior Cutaneous Nerve Entrapment Syndrome Peer-reviewed

    Yoshitaka Kondo, Nobuhiko Kanaya, Ami Kobayashi, Kyosuke Arakawa, Yoshikazu Matsuoka, Yudai Mimata, Yoshihiko Kakiuchi, Kunitoshi Shigeyasu, Shinji Kuroda, Shunsuke Kagawa, Toshiyoshi Fujiwara

    Neurology and Clinical Neuroscience (0) 1-7 2025/03/17

    Publisher: Wiley

    DOI: 10.1111/ncn3.70008  

    ISSN: 2049-4173

    eISSN: 2049-4173

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    ABSTRACT Background Anterior cutaneous nerve entrapment syndrome (ACNES) is often overlooked as a cause of chronic abdominal pain. Trigger point injections (TPIs) serve as both a diagnostic and therapeutic tool. Although neurectomy is frequently chosen for patients with severe ACNES, its surgical outcomes remain unclear. Aim This study aims to evaluate both the short‐ and long‐term outcomes for neurectomy and propose a novel therapeutic algorithm. Methods A cohort of postoperative patients presenting with ACNES between 2016 and 2023 was retrospectively evaluated. Patients received a single diagnostic TPI. When the pain subsided, an anterior neurectomy was performed using either an anterior or laparoscopic approach. Pain scores were assessed using the numeric rating scale (NRS). Results Among 37 patients (60% females, mean age 33.8 ± 3.4 years), 29 patients (78.4%) experienced pain recurrence following initial neurectomy. Of these, 22 patients underwent repeat neurectomies, resulting in complete remission in 15 patients and no benefit in 7 patients. Long‐term outcomes showed that 62.2% achieved clinical remission (NRS = 0), whereas 8.1% reported reduced but persistent pain (NRS 1–2). Preoperative TPI effectiveness was a strong predictor of surgical success, with patients achieving post‐TPI NRS (0–1) significantly more likely to attain remission (p = 0.0074). Older age was also associated with higher remission rates (p = 0.0476). Conclusion TPI is critical for predicting neurectomy success. These findings support the integration of preoperative TPI evaluation and tailored surgical strategies to optimize outcomes for patients with ACNES.

  10. Molecular biology and novel therapeutics for IDH mutant gliomas: The new era of IDH inhibitors. International-journal Peer-reviewed

    Yosuke Kitagawa, Ami Kobayashi, Daniel P Cahill, Hiroaki Wakimoto, Shota Tanaka

    Biochimica et biophysica acta. Reviews on cancer 1879 (3) 189102-189102 2024/04/21

    DOI: 10.1016/j.bbcan.2024.189102  

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    Gliomas with Isocitrate dehydrogenase (IDH) mutation represent a discrete category of primary brain tumors with distinct and unique characteristics, behaviors, and clinical disease outcomes. IDH mutations lead to aberrant high-level production of the oncometabolite D-2-hydroxyglutarate (D-2HG), which act as a competitive inhibitor of enzymes regulating epigenetics, signaling pathways, metabolism, and various other processes. This review summarizes the significance of IDH mutations, resulting upregulation of D-2HG and the associated molecular pathways in gliomagenesis. With the recent finding of clinically effective IDH inhibitors in these gliomas, this article offers a comprehensive overview of the new era of innovative therapeutic approaches based on mechanistic rationales, encompassing both completed and ongoing clinical trials targeting gliomas with IDH mutations.

  11. Emerging Roles and Mechanisms of RNA Modifications in Neurodegenerative Diseases and Glioma Invited Peer-reviewed

    Ami Kobayashi, Yosuke Kitagawa, Ali Nasser, Hiroaki Wakimoto, Keisuke Yamada, Shota Tanaka

    Cells 2024/03/05

    DOI: 10.3390/cells13050457  

  12. タウ蛋白と結合するtRNA断片はアルツハイマー型認知症におけるタウ凝集体形成を促進する

    小林天美, KHAREL Prakash, WILIAMS Allison, ZHANG Yanhong, IVANOV Pavel, KRICHEVKSY Anna

    日本生物学的精神医学会(Web) 46th 2024

  13. Roles of Noncoding RNAs in Regulation of Mitochondrial Electron Transport Chain and Oxidative Phosphorylation International-journal Invited Peer-reviewed

    Ami Kobayashi, Toshihiko Takeiwa, Kazuhiro Ikeda, Satoshi Inoue

    International Journal of Molecular Sciences 24 (11) 2023/05/28

    DOI: 10.3390/ijms24119414  

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    The mitochondrial electron transport chain (ETC) plays an essential role in energy production by inducing oxidative phosphorylation (OXPHOS) to drive numerous biochemical processes in eukaryotic cells. Disorders of ETC and OXPHOS systems are associated with mitochondria- and metabolism-related diseases, including cancers; thus, a comprehensive understanding of the regulatory mechanisms of ETC and OXPHOS systems is required. Recent studies have indicated that noncoding RNAs (ncRNAs) play key roles in mitochondrial functions; in particular, some ncRNAs have been shown to modulate ETC and OXPHOS systems. In this review, we introduce the emerging roles of ncRNAs, including microRNAs (miRNAs), transfer-RNA-derived fragments (tRFs), long ncRNAs (lncRNAs), and circular RNAs (circRNAs), in the mitochondrial ETC and OXPHOS regulation.

  14. A FRET-based respirasome assembly screen identifies spleen tyrosine kinase as a target to improve muscle mitochondrial respiration and exercise performance in mice Peer-reviewed

    Ami Kobayashi, Kotaro Azuma, Toshihiko Takeiwa, Toshimori Kitami, Kuniko Horie, Kazuhiro Ikeda, Satoshi Inoue

    Nature Communications 2023/01/25

    DOI: 10.1038/s41467-023-35865-x  

  15. 呼吸鎖超複合体形成による骨格筋のミトコンドリア機能調節とその制御因子

    小林天美, 小林天美

    基礎老化研究 46 (1) 2022

    ISSN: 0912-8921

  16. tRNA断片を介した神経細胞内タウ蛋白凝集の誘導と凝集体細胞間伝播機構

    小林天美, NGUYEN Lien, ZHANG Yanghong, DEFORZH Evgeny, UHLMANN Eric, KRICHEVSKY Anna

    Dementia Japan 36 (4) 2022

    ISSN: 1342-646X

  17. Mechanisms Underlying the Regulation of Mitochondrial Respiratory Chain Complexes by Nuclear Steroid Receptors Invited Peer-reviewed

    Ami Kobayashi, Kotaro Azuma, Kazuhiro Ikeda, Satoshi Inoue

    International Journal of Molecular Sciences 21 (18) 6683-6683 2020/09/12

    Publisher: {MDPI} {AG}

    DOI: 10.3390/ijms21186683  

    ISSN: 1422-0067

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    <jats:p>Mitochondrial respiratory chain complexes play important roles in energy production via oxidative phosphorylation (OXPHOS) to drive various biochemical processes in eukaryotic cells. These processes require coordination with other cell organelles, especially the nucleus. Factors encoded by both nuclear and mitochondrial DNA are involved in the formation of active respiratory chain complexes and ‘supercomplexes’, the higher-order structures comprising several respiratory chain complexes. Various nuclear hormone receptors are involved in the regulation of OXPHOS-related genes. In this article, we review the roles of nuclear steroid receptors (NR3 class nuclear receptors), including estrogen receptors (ERs), estrogen-related receptors (ERRs), glucocorticoid receptors (GRs), mineralocorticoid receptors (MRs), progesterone receptors (PRs), and androgen receptors (ARs), in the regulatory mechanisms of mitochondrial respiratory chain complex and supercomplex formation.</jats:p>

  18. 認知機能低下を主症状とし3カ月の経過で急激な一側性大脳半球の萎縮を呈した大脳皮質基底核変性症の1例

    小林天美, 旭俊臣

    日本老年医学会雑誌 56 (4) 2019

    ISSN: 0300-9173

  19. 超高齢社会に向けて:骨格筋と老化研究最前線 6.ミトコンドリアからみた骨格筋の老化

    小林天美, 東浩太郎, 池田和博, 井上聡, 井上聡

    実験医学 36 (7) 2018

    ISSN: 0288-5514

  20. The inverse correlation between anti cardiolipin β2- glycoproteini complex antibody tighter and hemorrhage risk prediction scores in ischemic stroke patients with antiphospholipid syndrome Peer-reviewed

    A. Kobayashi, J. Otsuka, A. Hida, N. Arai, S. Takeuchi, H. Yamashita, H. Kaneko

    Journal of the Neurological Sciences 381 648-648 2017/10

    Publisher: Elsevier {BV}

    DOI: 10.1016/j.jns.2017.08.1824  

    ISSN: 0022-510X

  21. 木村病を有し若年性脳梗塞を発症した32歳男性例

    大塚十里, 金蒼美, 小林天美, 肥田あゆみ, 新井憲俊, 萩原將太郎, 竹内壯介

    臨床神経学(Web) 57 (4) 2017

    ISSN: 1882-0654

  22. 多発脳神経麻痺で発症した眼窩内原発ATLの1例

    大草翔平, 大塚十里, 肥田あゆみ, 大森亜希, 川尻紘平, 氏家岳斗, 小林天美, 栂野富輝, 芳田奈津代, 竹内壯介

    日本内科学会関東支部関東地方会 626th 2016

  23. 多発筋炎に対しメソトレキサートを導入後,CK上昇を伴わない進行性の頸部四肢筋力低下,全身性皮疹及び筋腫瘤が出現した36歳男性例

    小口絢子, 小林天美, 山口奈々香, 羽尾暁人, 上田順子, 田島将吾, 清水潤, 辻省次

    臨床神経学(Web) 56 (2) 2016

    ISSN: 1882-0654

  24. 非定型抗酸菌症治療中にANCA関連血管炎による腎炎の再燃が疑われた1例

    小林天美, 本田謙次郎, 藤澤まどか, 菅原真衣, 中村元信, 新谷裕加子, 深山正久, 藤乘嗣泰, 南学正臣

    日本内科学会関東支部関東地方会 611th 2014

  25. ポリプテルスのHox遺伝子の単離と解析

    小林天美, 岡部正隆

    東京慈恵会医科大学雑誌 125 (6) 2010

    ISSN: 0375-9172

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Misc. 10

  1. tRNA断片を介した神経細胞内タウ蛋白凝集の誘導と凝集体細胞間伝播機構

    小林 天美, Nguyen Lien, Zhang Yanghong, Deforzh Evgeny, Uhlmann Eric, Krichevsky Anna

    老年精神医学雑誌 33 (増刊II) 221-222 2022/11

    Publisher: (株)ワールドプランニング

    ISSN: 0915-6305

  2. tRNA断片を介した神経細胞内タウ蛋白凝集の誘導と凝集体細胞間伝播機構

    小林 天美, Nguyen Lien, Zhang Yanghong, Deforzh Evgeny, Uhlmann Eric, Krichevsky Anna

    Dementia Japan 36 (4) 741-741 2022/10

    Publisher: (一社)日本認知症学会

    ISSN: 1342-646X

  3. 呼吸鎖超複合体形成による骨格筋のミトコンドリア機能調節とその制御因子

    小林 天美

    基礎老化研究 46 (1) 37-41 2022/01

    Publisher: 日本基礎老化学会

    ISSN: 0912-8921

  4. 認知機能低下を主症状とし3ヵ月の経過で急激な一側性大脳半球の萎縮を呈した大脳皮質基底核変性症の1例

    小林 天美, 旭 俊臣

    日本老年医学会雑誌 56 (4) 550-550 2019/10

    Publisher: (一社)日本老年医学会

    ISSN: 0300-9173

  5. 【超高齢社会に挑む骨格筋のメディカルサイエンス 筋疾患から代謝・全身性制御へと広がる筋研究を、健康寿命の延伸につなげる】(序章)超高齢社会に向けて 骨格筋と老化研究最前線 ミトコンドリアからみた骨格筋の老化

    小林 天美, 東 浩太郎, 池田 和博, 井上 聡

    実験医学 36 (7) 1102-1108 2018/05

    Publisher: (株)羊土社

    ISSN: 0288-5514

  6. 木村病を有し若年性脳梗塞を発症した32歳男性例

    大塚 十里, 金 蒼美, 小林 天美, 肥田 あゆみ, 新井 憲俊, 萩原 將太郎, 竹内 壯介

    臨床神経学 57 (4) 191-191 2017/04

    Publisher: (一社)日本神経学会

    ISSN: 0009-918X

    eISSN: 1882-0654

  7. 多発脳神経麻痺で発症した眼窩内原発ATLの1例

    大草 翔平, 大塚 十里, 肥田 あゆみ, 大森 亜希, 川尻 紘平, 氏家 岳斗, 小林 天美, 栂野 富輝, 芳田 奈津代, 竹内 壯介

    日本内科学会関東地方会 626回 62-62 2016/09

    Publisher: 日本内科学会-関東地方会

  8. 多発筋炎に対しメソトレキサートを導入後、CK上昇を伴わない進行性の頸部四肢筋力低下、全身性皮疹及び筋腫瘤が出現した36歳男性例

    小口 絢子, 小林 天美, 山口 奈々香, 羽尾 暁人, 上田 順子, 田島 将吾, 清水 潤, 辻 省次

    臨床神経学 56 (2) 128-128 2016/02

    Publisher: (一社)日本神経学会

    ISSN: 0009-918X

    eISSN: 1882-0654

  9. 非定型抗酸菌症治療中にANCA関連血管炎による腎炎の再燃が疑われた1例

    小林 天美, 本田 謙次郎, 藤澤 まどか, 菅原 真衣, 中村 元信, 新谷 裕加子, 深山 正久, 藤乗 嗣泰, 南学 正臣

    日本内科学会関東地方会 611回 28-28 2014/12

    Publisher: 日本内科学会-関東地方会

  10. ポリプテルスのHox遺伝子の単離と解析

    小林 天美, 岡部 正隆

    東京慈恵会医科大学雑誌 125 (6) 223-224 2010/11

    Publisher: 東京慈恵会医科大学成医会

    ISSN: 0375-9172

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Books and Other Publications 1

  1. 超高齢社会に挑む骨格筋のメディカルサイエンス : 筋疾患から代謝・全身性制御へと広がる筋研究を、健康寿命の延伸につなげる

    武田, 伸一

    羊土社 2018/05

    ISBN: 9784758103701

Presentations 15

  1. tRNA-derived fragments elevated in Alzheimer's disease facilitate Tau aggregation

    2026/05/22

  2. tRNA-derived fragments elevated in Alzheimer’s disease promote Tau aggregation Invited

    ARCND AD/PD 2026 SEMINAR SERIES 2026/01/27

  3. tRNA-derived fragments do not affect alpha-synuclein aggregation but specifically promote tau aggregate formation

    Ami Kobayashi

    2025/07/24

  4. RNA cofactors facilitating tau aggregation in Alzheimer’s disease Invited

    Ami Kovbayashi

    ARCND AD/PD 2024 SEMINAR SERIES 2024/11/26

  5. tRNA fragments that bind to tau protein promote tau aggregation in Alzheimer's disease

    Ami Kobayashi

    Neuro2024 2024/07/27

  6. tRNA-derived fragments function as tau binders, accelerating tau aggregation in Alzheimer's disease

    Ami Kobayashi

    65th Annual Meeting of the Japanese Society of Neurology and 19th Asian Ocenian Congress of Neurology 2024/06/01

  7. Regulation and Detection of the Modulation of Mitochondrial Respiratory Chain and Oxidative Phosphorylation Invited

    Ami Kobayashi

    The 2nd World Chemistry Congress 2024/05/23

  8. DISCOVERY OF SMALL RNA SPECIES UNDERLYING TAU AGGREGATION AND PATHOLOGY

    Ami Kobayashi

    18th International Conference on Alzheimer’s and Parkinson’s Diseases 2024/03/06

  9. The role of stress-induced tRNA-derived fragments in tau aggregation and propagation in Alzheimer's disease Invited

    Ami Kobayashi

    International Society of Neurochemistry Biennal Meeting 2023/08/09

  10. tRNA 断片を介した神経細胞内タウ蛋白凝集の誘導と凝集体細胞間伝播メカニズムの解明

    小林 天美

    第64回日本神経病理学会総会学術研究会/ 第66回日本神経化学会大会 合同大会 2023/07/06

  11. Tau binders: discovery of small RNA species underlying tau aggregation and pathology Invited

    Ami Kobayashi

    Tau Consortium Investigator’s Meeting 2023/07

  12. Discovery of RNA cofactors underlying tau aggregation and pathology in neurodegenerative diseases Invited

    Ami Kobayashi

    ARCND AD/PD 2023 SEMINAR SERIES 2023/02/14

  13. FRET-based high-throughput screen identifies a compound that promotes mitochondrial function by respiratory chain supercomplex assembly

    Ami Kobayashi

    2021/05

  14. 肺動静脈瘻を有し脳塞栓を繰り返した 68 歳女性例

    小林 天美

    第 17 回首都圏脳卒中フォーラム 2017/03

  15. 非定型抗酸菌症治療中に ANCA 関連血管炎による腎炎の再燃が疑われた 1 例

    小林 天美

    第 611 回日本内科学会関東地方会 2015/12

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Industrial Property Rights 2

  1. ミトコンドリア超複合体の形成促進剤、筋力維持又は増進用組成物、及び筋機能低下若しくはミトコンドリア機能低下疾患の治療又は予防用医薬組成物、並びにミトコンドリアの超複合体の形成に関与する物質のスクリーニング方法

    井上 聡, 東 浩太郎, 小林 天美

    Property Type: Patent

  2. Targeting tRNA-derived fragments for reducing tau pathology in Alzheimer's disease and related tauopathies

    Anna Krichevsky, Ami Kobayashi

    Property Type: Patent

Research Projects 6

  1. タウ蛋白凝集と細胞間伝播を制御するtRNA断片を標的とした神経変性疾患治療の開発

    Offer Organization: 公益財団法人 武田科学振興財団

    System: ビジョナリーリサーチ助成

    2026/08 - 2031/03

  2. tRNA断片を介した神経細胞内タウ蛋白凝集の誘導と細胞間伝播機構の解明

    Offer Organization: 公益財団法人三菱財団

    System: 自然科学研究若手助成

    2027/04 -

  3. tRNA断片を介した神経細胞内タウ蛋白凝集の誘導と細胞間伝播機構の解明

    Offer Organization: 公益信託成茂神経科学研究助成基金

    System: 令和8年度研究助成金

    2026/07 - 2027/03

  4. 運動による認知症発症予防効果に関わるミトコンドリア機能制御メカニズムの解明

    Offer Organization: 一般財団法人ヘルス・サイエンス・センター

    System: 2025年度研究助成金

    2026/03 - 2027/02

  5. 運動による認知症発症予防効果に関わるミトコンドリア機能調節因子と機序の解明

    Offer Organization: 公益財団法人 明治安田厚生事業団

    System: 若手研究者のための健康科学研究助成

    Institution: ハーバード大学医学部

    2023/11 - 2026/01

  6. tRNA断片を標的としたタウ蛋白凝集・細胞間伝播の制御による神経変性疾患薬治療の開発

    Offer Organization: 公益財団法人 金原一郎医学医療振興財団

    System: 基礎医学医療研究助成

    2024/10 - 2025/09

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