Updated on 2024/10/18

写真a

 
MATSUMOTO Shin-Ei
 
Organization
Research Field in Medicine and Health Sciences, Medical and Dental Sciences Area Graduate School of Medical and Dental Sciences Health Research Course Infection and Immunity Assistant Professor
Title
Assistant Professor
Degree
(2006.3 Kyushu University)
(2003.3 Kyushu University)
(2001.3 Kyushu University)

Research Interests

  • Alzheimer's disease

  • microglia

  • macrophage

Research Areas

Neurology, Molecular biology

Education

  • - 2006.3    Kyushu University

  • - 2003.3    Kyushu University

  • - 2001.3    Kyushu University

Research History

  • 2016.4    Kagoshima University   Research Field in Medicine and Health Sciences, Medical and Dental Sciences Area Graduate School of Medical and Dental Sciences Health Research Course Infection and Immunity   Assistant Professor

Professional Memberships

  • 2010.4    日本認知症学会

 

Papers

  • Sonoda R., Kuramoto E., Minami S., Matsumoto S.E., Ohyagi Y., Saito T., Saido T., Noguchi K., Goto T. .  Reduced Autophagy in Aged Trigeminal Neurons Causes Amyloid β Diffusion .  Journal of Dental Research102 ( 8 ) 938 - 946   2023.7

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    Language：Japanese   Publisher：Journal of Dental Research  

    The relationship between oral health and the development of Alzheimer’s disease (AD) in the elderly is not yet well understood. In this regard, the association between aging or neurodegeneration of the trigeminal nervous system and the accumulation of amyloid-β(1–42) (Aβ42) oligomers in the pathogenesis of AD is unknown. We focused on selective autophagy in the trigeminal mesencephalic nucleus (Vmes) and the diffusion of Aβ42 oligomers with respect to aging of the trigeminal nervous system and whether the degeneration of Vmes neurons affects the diffusion of Aβ42 oligomers. We used female 2- to 8-mo-old transgenic 3xTg-AD mice and AppNL-G-F knock-in mice and immunohistochemically examined aging-related changes in selective autophagy and Aβ42 oligomer processing in the Vmes, which exhibits high amyloid-β (Aβ) expression. We induced degeneration of Vmes neurons by extracting the maxillary molars and examined the changes in Aβ42 oligomer kinetics. Autophagosome-like membranes, which stained positive for Aβ, HO-1, and LC3B, were observed in Vmes neurons of 3xTg-AD mice, while there was weak immunoreactivity of the membranes for intraneuronal Aβ in AppNL-G-F mice. By contrast, there was strong immunopositivity for extracellular Aβ42 oligomers with the formation of Aβ42 oligomer clusters in AppNL-G-F mice. The expression of Rubicon, which indicates age-related deterioration of autophagy, increased the diffusion of Aβ42 oligomer with the age of Vmes neurons. Tooth extraction increased the extracellular immunopositivity for Aβ42 oligomers in AppNL-G-F mice. These results suggest that autophagy maintains homeostasis in Vmes neurons and that deterioration of autophagy due to aging or neurodegeneration leads to the diffusion of Aβ42 oligomers into the extracellular space and possibly the development of AD.

    DOI： 10.1177/00220345231156095

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  • 後藤 哲哉, 倉本 恵梨子, 北脇 綾乃, 河野 博史, 松本 信英, 原 博満, 八木 孝和, 大八木 保政, 岩井 治樹, 山中 淳之 .  アルツハイマー病モデルマウスを使った口腔フレイル解析システムの開発 .  老年精神医学雑誌33 ( 増刊II ) 256 - 256   2022.11

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    Language：Japanese   Publisher：(株)ワールドプランニング  

  • 後藤 哲哉, 倉本 恵梨子, 北脇 綾乃, 河野 博史, 松本 信英, 原 博満, 八木 孝和, 大八木 保政, 岩井 治樹, 山中 淳之 .  アルツハイマー病モデルマウスを使った口腔フレイル解析システムの開発 .  Dementia Japan36 ( 4 ) 757 - 757   2022.10

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    Language：Japanese   Publisher：(一社)日本認知症学会  

  • Eriko Kuramoto, Ayano Kitawaki, Takakazu Yagi, Hiroshi Kono, Shin-Ei Matsumoto, Hiromitsu Hara, Yasumasa Ohyagi, Haruki Iwai, Atsushi Yamanaka, Tetsuya Goto .  Development of a system to analyze oral frailty associated with Alzheimer's disease using a mouse model .  Frontiers in Aging Neuroscience14   935033   2022.8

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    Language：Japanese   Publishing type：Research paper (scientific journal)   Publisher：Frontiers Media SA  

    The rapid aging of the population makes the detection and prevention of frailty increasingly important. Oral frailty has been proposed as a novel frailty phenotype and is defined as a decrease in oral function coexisting with a decline in cognitive and physical functions. Oral frailty has received particular attention in relation to Alzheimer's disease (AD). However, the pathomechanisms of oral frailty related to AD remain unknown. It is assumed that the mesencephalic trigeminal nucleus (Vmes), which controls mastication, is affected by AD pathology, and as a result, masticatory function may be impaired. To investigate this possibility, we included male 3 × Tg-AD mice and their non-transgenic counterpart (NonTg) of 3–4 months of age in the present study. Immunohistochemistry revealed amyloid-β deposition and excessive tau phosphorylation in the Vmes of 3 × Tg-AD mice. Furthermore, vesicular glutamate transporter 1-immunopositive axon varicosities, which are derived from Vmes neurons, were significantly reduced in the trigeminal motor nucleus of 3 × Tg-AD mice. To investigate whether the AD pathology observed in the Vmes affects masticatory function, we analyzed electromyography of the masseter muscle during feeding. The 3 × Tg-AD mice showed a significant delay in masticatory rhythm compared to NonTg mice. Furthermore, we developed a system to simultaneously record bite force and electromyography of masseter, and devised a new method to estimate bite force during food chewing in mice. Since the muscle activity of the masseter showed a high correlation with bite force, it could be accurately estimated from the muscle activity. The estimated bite force of 3 × Tg-AD mice eating sunflower seeds was predominantly smaller than that of NonTg mice. However, there was no difference in masseter weight or muscle fiber cross-sectional area between the two groups, suggesting that the decreased bite force and delayed mastication rhythm observed in 3 × Tg-AD mice were not due to abnormality of the masseter. In conclusion, the decreased masticatory function observed in 3 × Tg-AD mice was most likely caused by AD pathology in the Vmes. Thus, novel quantitative analyses of masticatory function using the mouse model of AD enabled a comprehensive understanding of oral frailty pathogenesis.

    DOI： 10.3389/fnagi.2022.935033

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  • Tsukasa Fujiki, Shin-Ei Matsumoto, Kenji Kishihara, Yoshinori Katakura .  Age-related functional decline of human B cells. .  Cytotechnology74 ( 2 ) 319 - 327   2022.4International journal

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

    This study aimed to investigate the changes in B cell functional decline and antigen sensitization with aging using two Epstein Barr virus (EBV)-immortalized human B cell lines, one from a 22-year-old man (EBV-B young) and the other from a 65-year-old man (EBV-B old). The activity of senescence-associated β-galactosidase, a marker of cellular senescence, was enhanced in the EBV-B old cells compared with EBV-B young cells. Moreover, the levels of p16, p21, IL-6, TNF-α, and TGF-β1, which are senescence-associated secretary phenotypes, were also increased in EBV-B old cells. In vitro immunization of EBV-B cells with β-lactoglobulin further showed that EBV-B old cells had a reduced cell population of naïve B cells than that of EBV-B young cells. Furthermore, HLA-DR expression, which is important for antigen presentation, was decreased in the EBV-B old cells. Comparative microarray analysis between EBV-B young and old cells also showed decreased expression of antibody genes, such as those of the heavy chain and light chain (κ chain). These results suggest that cellular senescence and decreased gene expression are responsible, at least in part, for the decline in B cell function and antigen sensitization capacity with aging, which ultimately impairs the function of the acquired immune system.

    DOI： 10.1007/s10616-021-00513-z

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  • Tetsuo Hayashi, Shotaro Shimonaka, Montasir Elahi, Shin-Ei Matsumoto, Koichi Ishiguro, Masashi Takanashi, Nobutaka Hattori, Yumiko Motoi .  Learning Deficits Accompanied by Microglial Proliferation After the Long-Term Post-Injection of Alzheimer's Disease Brain Extract in Mouse Brains. .  Journal of Alzheimer's disease : JAD79 ( 4 ) 1701 - 1711   2021International journal

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

    BACKGROUND: Human tauopathy brain injections into the mouse brain induce the development of tau aggregates, which spread to functionally connected brain regions; however, the features of this neurotoxicity remain unclear. One reason may be short observational periods because previous studies mostly used mutated-tau transgenic mice and needed to complete the study before these mice developed neurofibrillary tangles. OBJECTIVE: To examine whether long-term incubation of Alzheimer's disease (AD) brain in the mouse brain cause functional decline. METHODS: We herein used Tg601 mice, which overexpress wild-type human tau, and non-transgenic littermates (NTg) and injected an insoluble fraction of the AD brain into the unilateral hippocampus. RESULTS: After a long-term (17-19 months) post-injection, mice exhibited learning deficits detected by the Barnes maze test. Aggregated tau pathology in the bilateral hippocampus was more prominent in Tg601 mice than in NTg mice. No significant changes were observed in the number of Neu-N positive cells or astrocytes in the hippocampus, whereas that of Iba-I-positive microglia increased after the AD brain injection. CONCLUSION: These results potentially implicate tau propagation in functional decline and indicate that long-term changes in non-mutated tau mice may reflect human pathological conditions.

    DOI： 10.3233/JAD-201002

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  • Shotaro Shimonaka, Shin-Ei Matsumoto, Montasir Elahi, Koichi Ishiguro, Masato Hasegawa, Nobutaka Hattori, Yumiko Motoi .  Asparagine residue 368 is involved in Alzheimer's disease tau strain-specific aggregation .  Journal of Biological Chemistry295 ( 41 ) 13996 - 14014   2020.10Reviewed

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  • Shotaro Shimonaka, Shin-Ei Matsumoto, Montasir Elahi, Koichi Ishiguro, Masato Hasegawa, Nobutaka Hattori, Yumiko Motoi .  Asparagine residue 368 is involved in Alzheimer's disease tau strain-specific aggregation. .  The Journal of biological chemistry295 ( 41 ) 13996 - 14014   2020.10

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    In tauopathies, tau forms pathogenic fibrils with distinct conformations (termed "tau strains") and acts as an aggregation "seed" templating the conversion of normal tau into isomorphic fibrils. Previous research showed that the aggregation core of tau fibril covers the C-terminal region (243-406 amino acids (aa)) and differs among the diseases. However, the mechanisms by which distinct fibrous structures are formed and inherited via templated aggregation are still unknown. Here, we sought to identify the key sequences of seed-dependent aggregation. To identify sequences for which deletion reduces tau aggregation, SH-SY5Y cells expressing a series of 10 partial deletion (Del 1-10, covering 244-400 aa) mutants of tau-CTF24 (243-441 aa) were treated with tau seeds prepared from a different tauopathy patient's brain (Alzheimer's disease, progressive supranuclear palsy, and corticobasal degeneration) or recombinant tau, and then seed-dependent tau aggregation was assessed biochemically. We found that the Del 8 mutant lacking 353-368 aa showed significantly decreased aggregation in both cellular and in vitro models. Furthermore, to identify the minimum sequence responsible for tau aggregation, we systematically repeated cellular tau aggregation assays for the delineation of shorter deletion sites and revealed that Asn-368 mutation suppressed tau aggregation triggered by an AD tau seed, but not using other tauopathy seeds. Our study suggested that 353-368 aa is a novel aggregation-responsible sequence other than PHF6 and PHF6*, and within this sequence, the Asn-368 residue plays a role in strain-specific tau aggregation in different tauopathies.

    DOI： 10.1074/jbc.RA120.013271

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  • Tetsuya Goto, Eriko Kuramoto, Ashis Dhar, Rachel Pei-Hsuan Wang, Haruka Seki, Haruki Iwai, Atsushi Yamanaka, Shin-Ei Matsumoto, Hiromitsu Hara, Makoto Michikawa, Yasumasa Ohyagi, Wai Keung Leung, Raymond Chuen-Chung Chang .  Neurodegeneration of Trigeminal Mesencephalic Neurons by the Tooth Loss Triggers the Progression of Alzheimer's Disease in 3×Tg-AD Model Mice .  Journal of Alzheimer's Disease76 ( 4 ) 1443 - 1459   2020.8Reviewed

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  • Tetsuya Goto, Eriko Kuramoto, Ashis Dhar, Rachel Pei-Hsuan Wang, Haruka Seki, Haruki Iwai, Atsushi Yamanaka, Shin-Ei Matsumoto, Hiromitsu Hara, Makoto Michikawa, Yasumasa Ohyagi, Wai Keung Leung, Raymond Chuen-Chung Chang .  Neurodegeneration of Trigeminal Mesencephalic Neurons by the Tooth Loss Triggers the Progression of Alzheimer's Disease in 3×Tg-AD Model Mice. .  Journal of Alzheimer's disease : JAD76 ( 4 ) 1443 - 1459   2020

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    BACKGROUND: The mesencephalic trigeminal nucleus (Vmes) is not only anatomically adjacent to the locus coeruleus (LC) but is also tightly associated with the function of the LC. The LC can be the first area in which Alzheimer's disease (AD) develops, although it is unclear how LC neuronal loss occurs. OBJECTIVE: We investigated whether neuronal death in the Vmes can be spread to adjacent LC in female triple transgenic (3×Tg)-AD mice, how amyloid-β (Aβ) is involved in LC neuronal loss, and how this neurodegeneration affects cognitive function. METHODS: The molars of 3×Tg-AD mice were extracted, and the mice were reared for one week to 4 months. Immunohistochemical analysis, and spatial learning/memory assessment using the Barnes maze were carried out. RESULTS: In 4-month-old 3×Tg-AD mice, aggregated cytotoxic Aβ42 was found in granules in Vmes neurons. Neuronal death in the Vmes occurred after tooth extraction, resulting in the release of cytotoxic Aβ42 and an increase in CD86 immunoreactive microglia. Released Aβ42 damaged the LC, in turn inducing a significant reduction in hippocampal neurons in the CA1 and CA3 regions receiving projections from the LC. Based on spatial learning/memory assessment, after the tooth extraction in the 4-month-old 3×Tg-AD mice, increased latency was observed in 5-month-old 3×Tg-AD mice 1 month after tooth extraction, which is similar increase of latency observed in control 8-month-old 3×Tg-AD mice. Measures of cognitive deficits suggested an earlier shift to dementia-like behavior after tooth extraction. CONCLUSION: These findings suggest that tooth extraction in the predementia stage can trigger the spread of neurodegeneration from the Vmes, LC, and hippocampus and accelerate the onset of dementia.

    DOI： 10.3233/JAD-200257

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  • Sachiko Nakayama, Shotaro Shimonaka, Montasir Elahi, Kenya Nishioka, Yutaka Oji, Shin-Ei Matsumoto, Yuanzhe Li, Hiroyo Yoshino, Kaoru Mogushi, Taku Hatano, Takeshi Sato, Teikichi Ikura, Nobutoshi Ito, Yumiko Motoi, Nobutaka Hattori .  Tau aggregation and seeding analyses of two novel MAPT variants found in patients with motor neuron disease and progressive parkinsonism. .  Neurobiology of aging84   240.e13 - 240.e22   2019.12

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    Variants in the microtubule-associated protein tau (MAPT) gene cause the genetic tauopathies, a subgroup of frontotemporal dementia (FTD) disorders. Through genetic screening of 165 cases possibly associated with tauopathies, including 88 Alzheimer's disease, 26 behavioral variant FTD, eight primary progressive aphasia, nine FTD with motor neuron disease, 21 progressive supranuclear palsy, and 13 corticobasal syndrome, we identified two novel MAPT variants: a heterozygous missense variant, p.P160S, in a patient with FTD with motor neuron disease and a heterozygous insertional variant, p.K298_H299insQ, in three patients with familial progressive supranuclear palsy. The corresponding recombinant tau proteins showed reduced microtubule assembly and increased aggregation by thioflavin S assay. Exon trapping analysis showed that p.K298_H299insQ resulted in the overproduction of 4-repeat tau. In a cell-based model, p.K298_H299insQ had both a higher aggregation ability and seeding activity compared with wild-type tau. These findings indicate that both p.P160S and p.K298_H299insQ may relate to neurodegeneration.

    DOI： 10.1016/j.neurobiolaging.2019.02.016

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  • Nakayama S, Shimonaka S, Elahi M, Nishioka K, Oji Y, Matsumoto SE, Li Y, Yoshino H, Mogushi K, Hatano T, Sato T, Ikura T, Ito N, Motoi Y, Hattori N .  Tau aggregation and seeding analyses of two novel MAPT variants found in patients with motor neuron disease and progressive parkinsonism. .  Neurobiology of aging   2019.3Reviewed

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  • Yuko Hara, Yumiko Motoi, Keigo Hikishima, Hiroshi Mizuma, Hirotaka Onoe, Shin-Ei Matsumoto, Montasir Elahi, Hideyuki Okano, Shigeki Aoki, Nobutaka Hattori .  Involvement of the Septo-Hippocampal Cholinergic Pathway in Association with Septal Acetylcholinesterase Upregulation in a Mouse Model of Tauopathy. .  Current Alzheimer research14 ( 1 ) 94 - 103   2017Invited Reviewed

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    Language：English   Publishing type：Research paper (scientific journal)   Publisher：BENTHAM SCIENCE PUBL LTD  

    BACKGROUND: Cholinergic cell loss in the basal forebrain, the major source of hippocampal cholinergic projections, has been implicated in Alzheimer's disease. OBJECTIVE: To examine whether the septohippocampal pathway is involved in tauopathy model mice and to elucidate the tau-associated mechanism underlying cholinergic alteration. METHODS: Adult (6 to 8 months old) and old (16 to 18 months old) transgenic mice expressing wild-type human tau, Tg601, were examined using Ex vivo diffusion tensor magnetic resonance imaging (DTI) and 2-[18F]fluoro- 2-deoxy-D-glucose positron emission tomography (FDG-PET). Choline acetyltransferase (ChAT)-positive neurons in the medial septum (MS) were counted by stereological methods. Acetylcholinesterase (AChE) activity and AChE mRNA in 6 brain regions were measured. RESULTS: Ex vivo DTI revealed that the number of fractional anisotropy (FA) streamlines in the septohippocampal tract decreased with age in Tg601 mice. The FA value in the septum was lower in old Tg601 mice than in non-tg mice. A voxel-based statistical analysis of FDG-PET revealed the presence of low glucose uptake areas, involving the MS in adults, and spread over regions including the hippocampal dentate gyrus in old mice. In the MS, the number of choline acetyltransferase (ChAT)-positive neurons decreased in old Tg601 mice. AChE activity and AChE mRNA T transcripts were exclusively higher in the septum. CONCLUSION: The upregulation of AChE in the septum may result in the selective degeneration of the septohippocampal cholinergic pathway in the tauopathy mouse model.

    DOI： 10.2174/1567205013666160602235800

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  • Hideo Hara, Fumiko Ono, Shinichiro Nakamura, Shin-ei Matsumoto, Haifeng Jin, Nobutaka Hattori and Takeshi Tabira .  An Oral Aβ Vaccine Using a Recombinant Adeno-Associated Virus Vector in Aged Monkeys: Reduction in Plaque Amyloid and Increase in Aβ Oligomers .  Journal of Alzheimer's Disease54 ( 3 ) 1047 - 1059   2016.10Reviewed

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    DOI： 10.3233/JAD-160514

  • Montasir Elahi, Zafrul Hassan, Yumiko Motoi, Shin-Ei Matsumoto, Koichi Ishiguro, and Nobutaka Hattori .  Region-specific vulnerability to oxidative stress, neuroinflammation, and tau hyperphosphorylation in experimental diabetes mellitus mice .  Journal of Alzheimer’s Disease   2016.4Reviewed

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  • Montasir Elahi, Yumiko Motoi, Shin-Ei Matsumoto, Zafrul Hasan, Koichi Ishiguro, and Nobutaka Hattori .  Short-term treadmill exercise increased tau insolubility and neuroinflammation in tauopathy model mice .  Neuroscience Letters   2016.1Reviewed

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  • Shin-Ei Matsumoto, Yumiko Motoi, Koichi Ishiguro, Takeshi Tabira, Fuyuki Kametani, Masato Hasegawa, and Nobutaka Hattori .  The twenty-four KDa C-terminal tau fragment increases with aging in tauopathy mice: implications of prion-like properties .  Human Molecular Genetics   2015.9Reviewed

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  • Makiko Yamashita, Gakuro Harada, Shin-Ei Matsumoto, Yoshihiro Aiba, Akira Ichikawa, Tsukasa Fujiki, Miyako Udono, Shigeru Kabayama, Tadashi Yoshida, Pingbo Zhang, Hiroshi Fujii, Sanetaka Shirahata, and Yoshinori Katakura .  Suppression of immunoglobulin production in human peripheral blood mononuclear cells by monocytes via secretion of heavy-chain ferritin .  Immunobiology   2014.2Reviewed

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  • Kosuke Tomimatsu, Shin-Ei Matsumoto, Hayato Tanaka, Makiko Yamashita, Hidekazu Nakanishi, Kiichiro Teruya, Saiko Kazuno, Tomoya Kinjo, Takeki Hamasaki, Ken-ichi Kusumoto, Shigeru Kabayama, Yoshinori Katakura, and Sanetaka Shirahata .  A rapid screening and production method using a novel mammalian cell display to isolate human monoclonal antibodies .  Biochemical and biophysical research communications   2013.11Reviewed

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  • Gakuro Harada, Shin-Ei Matsumoto, Makiko Yamashita, Kaoru Fujii, Sanetaka Shirahata, and Yoshinori Katakura .  In vitro immunization of Epstein-Barr virus-immortalized B cells augments antigen-specific antibody production .  Cytotechnology   2013.8Reviewed

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  • Satomi Shiota, Hidenori Takekawa, Shin-Ei Matsumoto, Kazuya Takeda, Fariz Nurwidya, Yasuko Yoshioka, Fumiyuki Takahashi, Nobutaka Hattori, Takeshi Tabira, Hideki Mochizuki, and Kazuhisa Takahashi .  Chronic Intermittent Hypoxia/Reoxygenation Facilitate Amyloid-β Generation in Mice .  Journal of Alzheimer’s Disease   2013.7Reviewed

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  • Kohei Shimada, Yumiko Motoi, Koichi Ishiguro, Taiki Kambe, Shin-Ei Matsumoto, Masako Itaya, Miyuki Kunichika, Hideo Mori, Atsuko Shinohara, Momoko Chiba, Yoshikuni Mizuno, Takashi Ueno, and Nobutaka Hattori .  Long-term oral lithium treatment attenuates motor disturbance in tauopathy model mice: Implications of autophagy promotion .  Neurobiology of disease   2012.4Reviewed

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  • Tohru Hasegawa, Masayoshi Ichiba, Shin-Ei Matsumoto, Koji Kasanuki, Taku Hatano, Hiroshige Fujishiro, Eizo Iseki, Nobutaka Hattori, Tatsuo Yamada, and Takeshi Tabira .  Urinary homocysteic acid levels correlate with mini-mental state examination scores in Alzheimer's disease patients .  Journal of Alzheimer’s Disease   2012.3Reviewed

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  • Tsukasa Fujiki, Atsuji Tsuji, Shin-Ei Matsumoto, Makiko Yamashita, Kiichiro Teruya, Sanetaka Shirahata, and Yoshinori Katakura .  Generation of a human anti-tumor necrosis factor-α monoclonal antibody by in vitro immunization with a multiple antigen peptide .  Bioscience, biotechnology, and biochemistry   2010.9Reviewed

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  • Kosuke Tomimatsu, Shin-Ei Matsumoto, Makiko Yamashita, Kiichiro Teruya, Yoshinori Katakura, Shigeru Kabayama, and Sanetaka Shirahata .  Production of human monoclonal antibodies against Fc(epsilon)RI(alpha) by a method combining in vitro immunization with phage display .  Bioscience, biotechnology, and biochemistry   2009.7Reviewed

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  • Yeon Suk Jung, Shin-Ei Matsumoto, Yoshinori Katakura, Makiko Yamashita, Kosuke Tomimatsu, Shigeru Kabayama, Kiichiro Teruya, and Sanetaka Shirahata .  Generation of human monoclonal antibodies against Propionibacterium acnes by applying the phage display method to human peripheral blood mononuclear cells immunized in vitro .  Cytotechnology   2008.6Reviewed

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  • Shin-Ei Matsumoto, Makiko Yamashita, Yoshinori Katakura, Yoshihiro Aiba, Kosuke Tomimatsu, Shigeru Kabayama, Kiichiro Teruya, and Sanetaka Shirahata .  A rapid and efficient strategy to generate antigen-specific human monoclonal antibody by in vitro immunization and the phage display method .  Journal of Immunological Methods   2008.3Reviewed

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  • Makiko Yamashita, Yoshinori Katakura, Yoshihiro Aiba, Shin-Ei Matsumoto, Kazuko Morihara, Kiichiro Teruya, Akira Ichikawa, and Sanetaka Shirahata .  Involvement of IL-10 in the suppression of antibody production by in vitro immunized peripheral blood mononuclear cells .  Cytotechnology   2007.12Reviewed

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  • Takashi Tamura, Kosuke Tomimatsu, Yoshinori Katakura, Makiko Yamashita, Shin-Ei Matsumoto, Yoshihiro Aiba, Yeon Suk Jung, Yoshiichi Abe, Tsukasa Fujiki, Kiichiro Teruya, and Sanetaka Shirahata .  Anti-peptide antibody production elicited by in vitro immunization of human peripheral blood mononuclear cells .  Bioscience, biotechnology, and biochemistry   2007.12Reviewed

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  • Yeon Suk Jung, Shin-Ei Matsumoto, Makiko Yamashita, Kosuke Tomimatsu, Kiichiro Teruya, Yoshinori Katakura, and Sanetaka Shirahata .  Propionibacterium acnes acts as an adjuvant in in vitro immunization of human peripheral blood mononuclear cells .  Bioscience, biotechnology, and biochemistry   2007.8Reviewed

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  • Shin-Ei Matsumoto, Makiko Yamashita, Yoshinori Katakura, Eri Noguchi, Yoshihiro Aiba, Akira Ichikawa, Kiichiro Teruya, and Sanetaka Shirahata .  In vitro immunization can elicit the expansion of diverse repertoire of B cells from peripheral blood mononuclear cells .  Cytotechnology   2006.11Reviewed

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  • Yoshihiro Aiba, Makiko Yamashita, Yoshinori Katakura, Yuki Furukawa, Shin-Ei Matsumoto, Kousuke Tomimatsu, Kiichiro Teruya, and Sanetaka Shirahata .  Identification of genes involved in the suppression of antibody production from human peripheral blood lymphocytes .  Bioscience, biotechnology, and biochemistry   2006.4Reviewed

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MISC

  • 歯の喪失はアルツハイマー病モデルマウスの脳幹におけるM1型ミクログリア分化を促進する

    後藤 哲哉, ダール・アシス, 倉本 恵梨子, 岩井 治樹, 山中 淳之, 松本 信英, 原 博満

    Journal of Oral Biosciences Supplement   2018   398 - 398   2018.9

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    Publisher：(一社)歯科基礎医学会  

  • Tauopathy培養細胞モデルを用いたTauの凝集・伝播に関わるアミノ酸配列の同定

    下中 翔太郎, 松本 信英, 本井 ゆみ子, 服部 信孝

    Dementia Japan   31 ( 4 )   553 - 553   2017.10

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    Publisher：(一社)日本認知症学会  

  • 抜歯はアルツハイマー病モデルマウスの中脳路核神経細胞のタウ・リン酸化を誘導する

    後藤 哲哉, 倉本 恵梨子, Ashis Dhar, 岩井 治樹, 山中 淳之, 松本 信英, 原 博満, 道川 誠

    Journal of Oral Biosciences Supplement   2017   265 - 265   2017.9

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    Publisher：(一社)歯科基礎医学会  

  • アルツハイマー病モデルマウスの抜歯後の行動変化ならびに組織学的解析

    関 遥, Ashis Dhar, 岩井 治樹, 倉本 恵梨子, 山中 淳之, 後藤 哲哉, 松本 信英, 原 博満

    Journal of Oral Biosciences Supplement   2017   394 - 394   2017.9

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    Publisher：(一社)歯科基礎医学会  

Presentations

  • 松本信英、本井ゆみ子、石黒幸一、田平武、亀谷富由樹、長谷川成人、服部信孝   タウオパチーモデルマウスの加齢に伴い増加する新奇切断タウの伝播と機能解析  

    第34回日本認知症学会学術集会 

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    Event date： 2015.10

    Language：Japanese   Presentation type：Poster presentation  

    Venue：青森  

  • Shin-Ei Matsumoto, Yukako Hasegawa, Nobutaka Hattori, Takeshi Tabira   Development of mimotopes based on Abeta oligomer specific monoclonal antibody   International conference

    Alzheimer’s Association International Conference 2014 

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    Event date： 2014.7

    Language：English   Presentation type：Poster presentation  

    Venue：Copenhagen, Denmark  

  • 松本信英、本井ゆみ子、石黒幸一、田平武、亀谷富由樹、長谷川成人、服部信孝   A novel tau modification induces microtubule disassembly with aging in tauopathy model mice  

    第36回日本分子生物学会年会 

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    Event date： 2013.12

    Language：Japanese   Presentation type：Poster presentation  

    Venue：神戸  

  • Shin-Ei Matsumoto, Taiki Kambe, Yumiko Motoi, Koichi Ishiguro, Yukako Hasegawa, Takeshi Tabira, Fuyuki Kametani, Masato Hasegawa, Nobutaka Hattori   Truncated tau causes microtubule disassembly with aging in tauopathy model mice   International conference

    Alzheimer’s Association International Conference 2013 

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    Event date： 2013.7

    Language：English   Presentation type：Poster presentation  

    Venue：Boston, USA  

  • 松本信英、金海峰、武田和也、長谷川由果子、本井ゆみ子、服部信孝、田平武   アルツハイマー病治療に応用可能な抗体の開発  

    第53回日本神経学会学術大会シンポジウム 

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    Event date： 2012.5

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

    Venue：東京  

  • Shin-Ei Matsumoto, Haifeng Jin, Nobutaka Hattori, Takeshi Tabira   3.4A10 reduces Aβ oligomers and attenuates memory impairment in mouse models of Alzheimer’s disease   International conference

    Alzheimer’s Association International Conference 2011 

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    Event date： 2011.7

    Language：English   Presentation type：Poster presentation  

    Venue：Paris, France  

  • Shimonaka Shotaro, Matsumoto Shin-ei, Motoi Yumiko, Hattori Nobutaka   高い伝播活性をもつタウC末端領域の同定(The Identification of the Tau C-terminal Regions with High Propagation Activity)  

    順天堂醫事雑誌  2017.12  順天堂医学会

  • 細川 まゆ子, 松本 信英, 角田 正史, 横山 和仁   胎児期から発達期にかけてのフッ素曝露による学習記憶能力及び情動不安への影響  

    日本衛生学雑誌  2017.3  (一社)日本衛生学会

  • 後藤 哲哉, ダール・アシス , 倉本 恵梨子, 岩井 治樹, 山中 淳之, 松本 信英, 原 博満   歯の喪失はアルツハイマー病モデルマウスの脳幹におけるM1型ミクログリア分化を促進する  

    Journal of Oral Biosciences Supplement  2018.9  (一社)歯科基礎医学会

  • 後藤 哲哉, 倉本 恵梨子, Ashis Dhar, 松本 信英, 原 博満, 山中 淳之, 岩井 治樹, 大八木 保政, 道川 誠   歯の喪失はpre-dementiaからdementiaへの進行を早める  

    Dementia Japan  2019.10  (一社)日本認知症学会

  • 後藤 哲哉, 倉本 恵梨子, ダール・アシス , 松本 信英, 原 博満, 山中 淳之, 岩井 治樹, 道川 誠   歯の喪失がアルツハイマー病を誘発させるメカニズムについて  

    Dementia Japan  2018.9  (一社)日本認知症学会

  • 後藤 哲哉, 倉本 恵梨子, Ashis Dhar, 岩井 治樹, 山中 淳之, 松本 信英, 原 博満, 道川 誠   抜歯はアルツハイマー病モデルマウスの中脳路核神経細胞のタウ・リン酸化を誘導する  

    Journal of Oral Biosciences Supplement  2017.9  (一社)歯科基礎医学会

  • 細川 まゆ子, 松本 信英, 横山 和仁   妊娠期低濃度フッ素曝露による仔マウスの記憶学習能力の雌雄差  

    日本衛生学雑誌  2019.2  (一社)日本衛生学会

  • Shimonaka Shotaro, Matsumoto Shin-ei, Motoi Yumiko, Hattori Nobutaka   凝集体形成に関わるTau C末端配列の同定(The Identification of the Tau C-Terminal Sequences Involved in Aggregates Formation)  

    順天堂醫事雑誌  2018.12  順天堂医学会

  • Shimonaka Shotaro, Matsumoto Shin-ei, Motoi Yumiko, Hattori Nobutaka   タウ凝集体形成に関与するタウC末端配列の特定(The Identification of the Tau C-terminal Sequences Involved in Aggregates Formation)  

    順天堂醫事雑誌  2019.12  順天堂医学会

  • Nomoto Yusuke, Yasukawa Shinsuke, Iizasa Ei'ichi, Matsumoto Shin-ei, Furue Masutaka, Kanekura Takuro, Hara Hiromitsu   アレルギー　皮膚炎　CARD11形態異常変異はマウスにアトピー性皮膚炎を発症させた(Allergy-1: skin inflammation　Hypomorphic CARD11 mutation developed inflammatory atopic disorders in mice)  

    日本免疫学会総会・学術集会記録  2019.11  (NPO)日本免疫学会

  • 関 遥, Ashis Dhar, 岩井 治樹, 倉本 恵梨子, 山中 淳之, 後藤 哲哉, 松本 信英, 原 博満   アルツハイマー病モデルマウスの抜歯後の行動変化ならびに組織学的解析  

    Journal of Oral Biosciences Supplement  2017.9  (一社)歯科基礎医学会

  • 下中 翔太郎, 松本 信英, 本井 ゆみ子, 服部 信孝   TauのC末端領域における凝集責任配列の同定とその性質の解析  

    Dementia Japan  2018.9  (一社)日本認知症学会

  • 下中 翔太郎, 松本 信英, 本井 ゆみ子, 服部 信孝   TauのAsn368変異はAlzheimer病由来seedによる凝集のみを低下させる  

    Dementia Japan  2019.10  (一社)日本認知症学会

  • 下中 翔太郎, 松本 信英, 本井 ゆみ子, 服部 信孝   Tauopathy培養細胞モデルを用いたTauの凝集・伝播に関わるアミノ酸配列の同定  

    Dementia Japan  2017.10  (一社)日本認知症学会

  • 園田 怜美, 倉本 恵梨子, 松本 信英, 原 博満, 大八木 保政, 野口 和行, 後藤 哲哉   3xTg-ADマウスにおける神経細胞内アミロイドβの加齢変化について  

    Dementia Japan  2020.10  (一社)日本認知症学会

  • 園田 怜美, 倉本 恵梨子, 南 総一郎, 松本 信英, 原 博満, 大八木 保政, 斉藤 貴志, 西道 隆臣, 野口 和行, 後藤 哲哉   神経細胞における選択的オートファジーとAβオリゴマーの動態について  

    老年精神医学雑誌  2022.11  (株)ワールドプランニング

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    Language：Japanese  

  • 園田 怜美, 倉本 恵梨子, 松本 信英, 原 博満, 大八木 保政, 野口 和行, 後藤 哲哉   三叉神経中脳路核の神経変性によるアミロイドβオリゴマーの拡散について  

    Dementia Japan  2021.10  (一社)日本認知症学会

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    Language：Japanese  

  • 後藤 哲哉, 倉本 恵梨子, 北脇 綾乃, 河野 博史, 松本 信英, 原 博満, 八木 孝和, 大八木 保政, 岩井 治樹, 山中 淳之   アルツハイマー病モデルマウスを使った口腔フレイル解析システムの開発  

    老年精神医学雑誌  2022.11  (株)ワールドプランニング

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    Language：Japanese  

  • 園田 怜美, 倉本 恵梨子, 南 総一郎, 松本 信英, 原 博満, 大八木 保政, 斉藤 貴志, 西道 隆臣, 野口 和行, 後藤 哲哉   神経細胞における選択的オートファジーとAβオリゴマーの動態について  

    Dementia Japan  2022.10  (一社)日本認知症学会

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    Language：Japanese  

  • Matsumoto Shin-ei, Hara Hiromitsu   病原性マクロファージあるいは組織常在性マクロファージの発生に関する細胞基盤　CSFRs非依存的であるがTREM2依存的に誘導される骨髄由来マクロファージの特性解析(Cellular basis for the development of pathogenic or tissue-resident macrophages　Characterization of bone marrow-derived macrophages induced in a CSFRs-independent but TREM2-dependent manner)  

    日本免疫学会総会・学術集会記録  2023.12  (NPO)日本免疫学会

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    Language：English  

  • 後藤 哲哉, 倉本 恵梨子, 北脇 綾乃, 河野 博史, 松本 信英, 原 博満, 八木 孝和, 大八木 保政, 岩井 治樹, 山中 淳之   アルツハイマー病モデルマウスを使った口腔フレイル解析システムの開発  

    Dementia Japan  2022.10  (一社)日本認知症学会

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    Language：Japanese  

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Research Projects

  • コロニー刺激因子受容体非依存的・TREM2依存的な未知のマクロファージ分化機構の解明

    Grant number：24K10274  2024.4 - 2027.3

    日本学術振興会  科学研究費助成事業  基盤研究(C)

    松本 信英

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

  • Elucidation of the mechanism by which aging-induced deterioration of oral function is involved in the development of Alzheimer's disease.

    Grant number：23H03119  2023.4 - 2027.3

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

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    Grant amount：\18590000 （ Direct Cost: \14300000 、 Indirect Cost：\4290000 ）

  • Elucidation of the molecular mechanism by which neurodegeneration caused by tooth loss initiates Alzheimer's disease

    Grant number：20K10296  2020.4 - 2024.3

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

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

  • 凝集タウの伝播におけるミクログリアの役割の解明

    2019.4 - 2022.3

    科学研究費補助金  基盤研究(C)

  • 凝集タウの伝播におけるミクログリアの役割の解明

    2019.4 - 2021.3

    松本 信英

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    Authorship：Principal investigator  Grant type：Competitive

  • タウオパチー伝播モデルを用いたアルツハイマー病危険因子の役割の解明

    2016.4 - 2019.3

    科学研究費補助金  基盤研究(C)

  • タウオパチー伝播モデルを用いたアルツハイマー病危険因子の役割の解明

    2016.4 - 2018.3

    松本 信英

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