Tokushima University / Educator and Researcher Directory --- Nazere, Keyoumu

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Tokushima University ⟩ Graduate School of Biomedical Sciences ⟩ 医学域 ⟩ 先端基礎医学教育研究プロジェクト ⟩
Tokushima University ⟩ Graduate School of Biomedical Sciences ⟩ 医学域 ⟩ Medical Science ⟩ Physiological Sciences ⟩ 遺伝情報医学 ⟩
Tokushima University ⟩ Faculty of Medicine ⟩ School of Medicine ⟩ Course of Molecular Medicine ⟩ 遺伝情報医学分野 ⟩

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Research

Personal Web Page

https://researchmap.jp/nazira (researchmap)

Field of Study

○	Life sciences [Neuroscience - general]
○	Life sciences [Neurology]

Subject of Study

Book / Paper

(See https://researchmap.jp/nazira (researchmap) for Published Book / Papers / Presentations.)

Academic Paper (Judged Full Paper):

1.	Tomoyasu Matsubara, Naoki Kihara, Satoko Miyatake, Koji Fujita, Konoka Tachibana, Ryosuke Miyamoto, Hiroki Yamazaki, Yusuke Osaki, Keyoumu Nazere, Yuki Kuwano, Nobutoshi Morimoto, Suzuran Saito, Eriko Koshimizu, Yoichi Otomi, Kenji Ishibashi, Masafumi Harada, Naomichi Matsumoto, Hiroyuki Morino and Yuishin Izumi : TBK1-Associated Primary Lateral Sclerosis Followed by Right Temporal Variant Frontotemporal Dementia, Annals of Clinical and Translational Neurology, 2026. (Keyword) frontotemporal dementia / motor neuron disease / primary lateral sclerosis / TBK1 / TDP-43 (Link to Publication Site) ● Publication site (DOI): 10.1002/acn3.70329 (Link to Search Site for Scientific Articles) ● Summary page in Scopus @ Elsevier: 2-s2.0-105029388994 (DOI: 10.1002/acn3.70329, Elsevier: Scopus)
2.	Kazuki Muguruma, Tetsuya Takahashi, Yuichiro Tagane, Keyoumu Nazere, Naoyuki Hara, Masahiro Nakamori, Yu Yamazaki, Hiroyuki Morino and Hirofumi Maruyama : Intracellular anionic substances cause tau liquid-liquid phase separation., Biochemical and Biophysical Research Communications, 757, 2025. (Summary) Tau protein aggregation plays an important role in the pathophysiology of neurodegenerative diseases, including Alzheimer's disease and Niemann-Pick disease type C. Liquid-liquid phase separation has emerged as a key mechanism in the early stages of protein aggregation for these disorders. Tau protein incubated with heparin undergoes liquid-liquid phase separation to form liquid droplets in vitro. However, whether tau liquid droplet formation occurs in vivo remains unresolved. To investigate cellular conditions that promote tau droplet formation, we treated tau-expressing human embryonic kidney 293T cells with reagents that introduced anionic substances or induced intracellular vesicle accumulation. Suppression of Niemann-Pick disease type C1 protein, a lysosomal membrane protein involved in mediating intracellular cholesterol trafficking, or the introduction of negatively charged dextran into cultured cells, increased the formation of tau-positive puncta with liquid droplet characteristics in a concentration-dependent manner. After prolonged observation, these puncta transitioned from a dynamic liquid state to a more solid-like gel phase, indicating progressive aggregation. Our findings suggest that intracellular enrichment of negatively charged substances or vesicles induces tau phase separation, potentially contributing to its pathological aggregation. These results provide insight into the molecular mechanisms underlying tauopathies and highlight potential targets for therapeutic intervention. (Keyword) Humans / tau Proteins / HEK293 Cells / Anions / Protein Aggregation, Pathological / Heparin / Dextrans / phase transition / liquid-liquid phase separation (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbrc.2025.151605 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 40107109 ● Search Scopus @ Elsevier (PMID): 40107109 ● Search Scopus @ Elsevier (DOI): 10.1016/j.bbrc.2025.151605 (DOI: 10.1016/j.bbrc.2025.151605, PubMed: 40107109)
3.	Kenta Hanada, Yusuke Osaki, Ryosuke Miyamoto, Kohei Muto, Shotaro Haji, Keyoumu Nazere, Yuki Kuwano, Hiroyuki Morino, Yoshiteru Azuma, Satoko Miyatake, Naomichi Matsumoto and Yuishin Izumi : Intermediate phenotype between CMT2Z and DIGFAN associated with a novel MORC2 variant: a case report., Human Genome Variation, 11, 1, 29, 2024. (Summary) Charcot-Marie-Tooth disease type 2Z is caused by MORC2 mutations and presents with axonal neuropathy. MORC2 mutations can also manifest as developmental delay, impaired growth, dysmorphic facies, and axonal neuropathy (DIGFAN). We report a patient exhibiting an intermediate phenotype between these diseases associated with a novel MORC2 variant. A literature review revealed that the genotype‒phenotype correlation in MORC2-related disorders is complex and that the same mutation can cause a variety of phenotypes. (Tokushima University Institutional Repository) ● Metadata: 2012806 (Link to Publication Site) ● Publication site (DOI): 10.1038/s41439-024-00287-8 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 39143067 ● Summary page in Scopus @ Elsevier: 2-s2.0-85201316762 (Tokushima University Institutional Repository: 2012806, DOI: 10.1038/s41439-024-00287-8, PubMed: 39143067, Elsevier: Scopus)
4.	Takafumi Tomenaga, Shinobu Minatani, Hiroto Namba, Akitoshi Takeda, Takahito Yoshizaki, Joji Kawabe, Keyoumu Nazere, Hiroyuki Morino, Makoto Higuchi, Tomoyasu Matsubara, Hiroyuki Hatsuta, Masato Hasegawa, Shigeo Murayama and Yoshiaki Itoh : An autopsy case of type A FTLD-TDP with a GRN mutation presenting with the logopenic variant of primary progressive aphasia at onset and with corticobasal syndrome subsequently., Neuropathology, 2024. (Summary) A 68-year-old woman presented with difficulty finding words and writing characters. Neurological examination led to clinical diagnosis at onset of the logopenic variant of primary progressive aphasia accompanied with ideomotor apraxia, visuospatial agnosia on the right, and Gerstmann syndrome. Bradykinesia and rigidity on the right with shuffling gait developed after one year. Treatment with L-dopa had no effect. The patient was diagnosed with corticobasal syndrome (CBS). Brain magnetic resonance imaging revealed diffuse cortical atrophy dominantly on the left, especially in the temporal, parietal, and occipital lobes. Positron emission tomography did not reveal any significant accumulation of amyloid β or tau protein. She died five years later. Neuropathological examination revealed diffuse cortical atrophy with severe neuronal loss and fibrous gliosis in the cortex. Neuronal cytoplasmic inclusions, short dystrophic neurites, and, most notably, neuronal intranuclear inclusions, all immunoreactive for phosphorylated TDP-43, were observed. Western blotting revealed a full length and fragments of phosphorylated TDP-43 at 45 and 23kDa, respectively, confirming the pathological diagnosis of type A FTLD-TDP. Whole exome sequencing revealed a pathogenic mutation in GRN (c.87dupC). FTLD-TDP should be included in the differential diagnosis of CBS. (Link to Publication Site) ● Publication site (DOI): 10.1111/neup.12980 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38715398 ● Search Scopus @ Elsevier (PMID): 38715398 ● Search Scopus @ Elsevier (DOI): 10.1111/neup.12980 (DOI: 10.1111/neup.12980, PubMed: 38715398)

Proceeding of International Conference:

1.	Yuki Kuwano, Keyoumu Nazere and Hiroyuki Morino : The biological role of m6A RNA methylation in cytoplasmic localization of TDP-43, 第65回日本神経学会学術大会/AOCN2024, May 2024.

Proceeding of Domestic Conference:

1.	tachibana konoka, muto kohe, Ryosuke Miyamoto, Yuki Kuwano, kihara naoki, Masaki Kamada, Banzai Seishu, Ueno Hiroki, Tatsuya Fukumoto, Keyoumu Nazere, Maruyama Hirofumi, Yuishin Izumi and Hiroyuki Morino : GIPC1 intermediate-length repeat expansion in amyotrophic lateral sclerosis, 日本人類遺伝学会第70回大会, Dec. 2025.
2.	Keyoumu Nazere, 高橋哲也 (名), Yuki Kuwano and Hiroyuki Morino : 細胞内アミロイドβはアルツハイマー病においてリソソーム恒常性を破綻させタウのリン酸化に影響を与える, 第48回日本分子生物学会年会, Dec. 2025.
3.	Yuki Kuwano, Keyoumu Nazere, Masaki Kamada and Hiroyuki Morino : m6A RNA methylation mediates cytoplasmic localization and pathogenicity of TDP-43, 第66回日本神経学会学術大会, May 2025.
4.	Masaki Kamada, Keyoumu Nazere, Yuki Kuwano and Hiroyuki Morino : パーキンソン病患者の死因について, 第66回日本神経学会学術大会, May 2025.
5.	MUTO Kohei, Ryosuke Miyamoto, Yuki Kuwano, Keyoumu Nazere, Tatsuya Fukumoto, TACHIBANA Konoka, YAMAUCHI Shoma, Masaki Kamada, Yuishin Izumi and Hiroyuki Morino : 筋萎縮性側索硬化症(ALS)患者における新規リピート異常伸長の探索, 第66回日本神経学会学術大会, May 2025.
6.	Yuki Kuwano, Keyoumu Nazere, OHAMA Nanako, TANIGUCHI Soru, Kensei Nishida, Masaki Kamada and Hiroyuki Morino : TRA2B promotes colon cancer progression via onco-microRNA biogenesis, 第46回日本分子生物学会年会, Nov. 2024.
7.	YAMAUCHI Shoma, TACHIBANA Konoka, Ryosuke Miyamoto, Nagako Murase, MUTO Kohei, Tatsuya Fukumoto, Yuki Kuwano, Keyoumu Nazere, Ryuji Kaji, Hiroyuki Morino and Yuishin Izumi : 本邦におけるVPS16ジストニア (DYT-VPS16) の臨床的特徴, 第65回日本神経学会学術大会/AOCN2024, Jun. 2024.
8.	Keyoumu Nazere, Konoka Tachibana, Yuki Kuwano, Ryosuke Miyamoto, Ryuji Kaji, Yuishin Izumi and Hiroyuki Morino : The identification and functional analysis of novel variants in ADCY5- related movement disorders, 第65回日本神経学会学術大会/AOCN2024, May 2024.
9.	MUTO Kohei, Ryosuke Miyamoto, Yuki Kuwano, Keyoumu Nazere, Tomoyasu Matsubara, Tatsuya Fukumoto, TACHIBANA Konoka, YAMAUCHI Shoma, Yuishin Izumi and Hiroyuki Morino : 筋萎縮性側索硬化症(ALS)患者における原因リピート伸長変異の探索, 第65回日本神経学会学術大会, May 2024.
10.	Yuki Kuwano, Keyoumu Nazere, Kensei Nishida and Hiroyuki Morino : 抗老化RNA uc.138 のm6Aメチル化修飾を介した大腸がん悪性化メカニズム, 第46回日本分子生物学会年会, Dec. 2023.
11.	YAMAUCHI Shoma, Ryosuke Miyamoto, MUTO Kohei, Yuki Kuwano, Keyoumu Nazere, Kensei Nishida, TACHIBANA Konoka, Yuishin Izumi and Hiroyuki Morino : Search for Pathogenic Variant of ALS by Prioritization based on Phenotype, 第64回日本神経学会学術大会, Jun. 2023.

Et cetera, Workshop:

1.	Yuki Kuwano, Keyoumu Nazere and Hiroyuki Morino : m6A RNAメチル化がトリガーするALS原因因子TDP-43の細胞質封入体形成の調節機構, 先端酵素学研究所交流シンポジウム, Aug. 2024.

Grants-in-Aid for Scientific Research (KAKEN Grants Database @ NII.ac.jp)

アミロイドβ内在化によるリソソームの機能障害の網羅的解析とタウ凝集への影響 (Project/Area Number: 25K19029 )
Search by Researcher Number (60976108)