Updated on 2024/10/04

Information

 

写真a

 
TAKE HIRO
 
Organization
Faculty of Dental Science Department of Dental Science Associate Professor
School of Dentistry Department of Dentistry（Concurrent）
Graduate School of Dental Science （Concurrent）
Graduate School of Dental Science Department of Dental Science（Concurrent）
Title
Associate Professor
Contact information
メールアドレス
Profile
Consistently for years, I have been researching the effects of chronic systemic inflammation including periodontal disease on the brain. I am promoting the elucidation of the signaling pathway of chronic systemic inflammation to the brain and the mechanism that influences it, and my research interests are the brain and systemic immune organs. As development of pathological mechanism elucidation, I am also searching for natural substances that “control inflammation”.
External link

Degree

  • Bachelor of Medicine

  • Master of Medical sciences

  • PｈD of Detal sciences

Research History

  • 吉林大学　　　　　（中国）　　歯学部　客員教授 中国医科大学　　　（中国）　　歯学部　客員教授 サウザンプトン大学（英国）　　客員研究員   

Research Interests・Research Keywords

  • Research theme： The roles of phagocytes in aging

    Keyword： aging phagocytes

    Research period： 2005.5 - 2010.5

  • Research theme： Impact ofchronic systemic brain inflammation on brain functions

    Keyword： systemic inflammation, neuroinflammation, neuroimmunity, leptomeningeal cell, brain aging

    Research period： 1996.10

Awards

  • Top cited article 2021-2022

    2023.1   Journal of Neurochemistry   Receptor for Advanced Glycation End Products Upregulation in Cerebral Endothelial Cells Mediates Cerebrovascular-related Amyloid β Accumulation After Porphyromonas Gingivalis Infection.

  • 第26回日本女性科学者の会奨励賞

    2021.3   日本女性科学者の会   歯周病のアルツハイマー型認知症への関与メカニズム解明

  • Best Poster Award

    2015.7   International Conference on Neurology & Therapeutics   Involvement of brain pericyte damage in neuropathological changes associated with lysosomal storage

Papers

  • GSK3β is involved in promoting Alzheimer’s disease pathologies following chronic systemic exposure to Porphyromonas gingivalis lipopolysaccharide in amyloid precursor proteinNL-F/NL-F knock-in mice. Reviewed International journal

    Muzhou Jiang, Xinwen Zhang, Xu Yan, Shinsuke Mizutani, Haruhiko Kashiwazaki, Junjun Ni† and Zhou Wu

    Brain Behav Immun.   98   1 - 12   2021.9

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

    DOI： 10.1016/j.bbi.2021.08.213

  • Porphyromonas gingivalis infection induces synaptic failure via increased IL-1βproduction in leptomeningeal cells Reviewed International journal

    Wanyi Huang, Fan Zeng, Yebo Gu, Muzhou Jiang, Xinwen Zhang, Xu Yan, Tomoko Kadowaki, Shinsuke Mizutani, Haruhiko Kashiwazaki, Junjun Ni† and Zhou Wu

    J. Alzheimer's Dis.   83 ( 2 )   665 - 681   2021.6

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

    DOI： 10.3233/JAD-210031.

  • Mediates Cerebrovascular-related Amyloid β Accumulation After Porphyromonas Gingivalis Infection Reviewed International journal

    Zng F, Liu Y, Huang W, Qing H, Kadowaki T, Kashiwazaki H, Ni J, Wu Z

    Journal of Neurochemistry   1 - 13   2020.6

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

    Cerebrovascular-related amyloidogenesis is found in over 80% of Alzheimer’s disease (AD) cases, and amyloid β (Aβ) generation is increased in the peripheral macrophages during infection of Porphyromonas gingivalis (P. gingivalis), a causal bacterium for periodontitis. In the present study, we focused on receptor for advanced glycation end products (RAGE), the key molecule involves in Aβ influx after P. gingivalis infection to test our hypothesis that Aβ transportation from periphery into the brain, known as “Aβ influx”, is enhanced by P. gingivalis infection. Using cultured hCMEC/D3 cell line, in comparison to uninfected cells, directly infection with P. gingivalis (multiplicity of infection, MOI=5) significantly increased a time-dependent RAGE expression resulting in a dramatic increase of Aβ influx in the hCMEC/D3 cells; the P. gingivalis-upregulated RAGE expression was significantly decreased by NF-κB and Cathepsin B (CatB)-specific inhibitors, and the P.gingivalis-increased IκBα degradation was significantly decreased by CatB specific inhibitor. Furthermore, the P. gingivalis-increased Aβ influx was significantly reduced by RAGE-specific inhibitor. Using 15-month-old mice (C57BL/6JJmsSlc, female), in comparison to non-infection mice, systemic P. gingivalis infection for 3 consecutive weeks (1×108 CFU/mouse, every 3 days, intraperitoneally) significantly increased the RAGE expression in the CD31-positive endothelial cells and the Aβ loads around the CD31-positive cells in the mice’s brains. The RAGE expression in the CD31-positive cells was positively correlated with the Aβ loads. These observations demonstrate that the upregulated RAGE expression in cerebral endothelial cells mediates the Aβ influx after P. gingivalis infection, and CatB plays a critical role in regulating the NF-κB/RAGE expression.

    DOI： 10.1111/jnc.15096

  • Cathepsin B Inhibition Blocks Neurite Outgrowth in Cultured Neurons by Regulating Lysosomal Trafficking and Remodeling Reviewed International journal

    Jiang M, Meng J, Zeng F, Qing H, Hook G, Hook V, Wu Z, Ni J

    Journal of Neurochemistry   1 - 13   2020.4

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

    DOI： 10.1111/jnc.15032

  • Porphyromonas gingivalis Infection Induces Amyloid-β Accumulation in Monocytes/Macrophages Reviewed International journal

    Nie, Ran; Wu, Zhou; Ni, Junjun; Zeng, Fan; Yu, Weixian; Zhang, Yufeng; Kadowaki, Tomoko ; Kashiwazaki, Haruhiko; Teeling, Jessica L. ; Zhou, Yanmin

    Journal of Alzheimer's Disease   2019.11

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

    Abnormal accumulations of amyloid-β (Aβ) in the brain is the most significant pathological hallmark of Alzheimer’s disease (AD), and we have found that chronic systemic exposure to lipopolysaccharide of P. gingivalis induces the brain Aβ accumulation in the middle-aged mice. On the other hand, recent research has shown that circulating Aβ are transferred into the brain, however, the involvement of chronic systemic P. gingivalis infection in peripheral Aβ metabolism is unknown. We hypothesized that chronic P. gingivalis infection expands the Aβ pools in peripheral inflammatory tissues which contributes to the accumulation of Aβ in the brain during periodontitis. We conducted immunofluorescence and biochemical analyses on the molecules of inflammation and Aβ metabolism in the chronic systemic P. gingivalis infected middle-aged mice and the P. gingivalis infected cultured monocyte/macrophages (RAW264.7 cells). We showed that the increased expressions of IL-1β, APP770, CatB, Aβ1-42 and Aβ3-42 were mainly co-localized with macrophages in the liver of P. gingivalis infected mice. Blocking CatB and NF-κB by their specific inhibitors significantly inhibited the P. gingivalis infection induced expressions of IL-1β, APP770, Aβ1-42 and Aβ3-42 in cultured RAW264.7 cells. Additionally, the expressions of APP770, CatB, Aβ1-42 and Aβ3-42 were determined in the macrophages of gingival tissues form patients of periodontitis. These findings indicate that chronic systemic P. gingivalis infection induces Aβ accumulation in the inflammatory monocytes/macrophages via activating CatB/NF-κB signaling, thus suggests monocytes/macrophages serve as a circulation Aβ pool during periodontitis. CatB should be a novel therapeutic target for preventing periodontitis-related AD initiation and pathology process.

  • Increased expression and altered subcellular distribution of cathepsin B in microglia induce cognitive impairment through oxidative stress and inflammatory response in mice Reviewed

    Junjun Ni, Hiro Take, Veronika Stoka, Jie Meng, Yoshinori Hayashi, Christoph Peters, Hong Qing, Vito Turk, Hiroshi Nakanishi

    Aging cell   18 ( 1 )   2019.2

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

    DOI： 10.1111/acel.12856

  • Brazilian Green Propolis Prevents Cognitive Decline into Mild Cognitive Impairment in Elderly People Living at High Altitude Reviewed International journal

    Zhu A, Wu Z, Zhong X, Ni J, Li Y, Meng J, Du C, Zhao X, Nakanishi H, Wu S

    J. Alzheimer's Dis   2018.6

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

  • Cathepsin B plays a critical role in inducing Alzheimer's disease-like phenotypes following chronic systemic exposure to lipopolysaccharide from Porphyromonas gingivalis in mice Reviewed International journal

    Hiro Take, Junjun Ni, Yicong Liu, Jessica L. Teeling, Fumiko Takayama, Alex Collcutt, Paul Ibbett, Hiroshi Nakanishi

    Brain, Behavior, and Immunity   65   350 - 361   2017.10

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

    DOI： 10.1016/j.bbi.2017.06.002

  • The Neuroprotective Effects of Brazilian Green Propolis on Neurodegenerative Damage in Human Neuronal SH-SY5Y Cells Reviewed

    Junjun Ni, Hiro Take, Jie Meng, Aiqin Zhu, Xin Zhong, Shizheng Wu, Hiroshi Nakanishi

    Oxidative Medicine and Cellular Longevity   2017   2017.1

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

    DOI： 10.1155/2017/7984327

  • The critical role of proteolytic relay through cathepsins B and E in the phenotypic change of microglia/macrophage Reviewed International journal

    NI JUNJUN, Wu Z, Christoph Peterts, Kenji, Yamamoto, Hong Qin, Hiroshi Nakanishi

    J. Neurosci   35 ( 36 )   12488 - 501   2015.9

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

    DOI： 10.1523/JNEUROSCI.1599-15.2015

  • Leptomeningeal cells transduce peripheral macrophages inflammatory signal to microglia in reponse to Porphyromonas gingivalis LPS. Reviewed International journal

    Liu Y, Wu Z, Zhang XW, Ni J, Yu W, Zhou Y, Hiroshi Nakanishi

    Mediators Inflamm.   2013.12

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

    DOI： 10.1155/2013/407562

  • Differential pathways for interleukin-1β production activated by chromogranin A and amyloid β in microglia Reviewed

    Hiro Take, Li Sun, Sadayuki Hashioka, Sheng Yu, Claudia Schwab, Ryo Okada, Yoshinori Hayashi, Patrick L. McGeer, Hiroshi Nakanishi

    Neurobiology of Aging   34 ( 12 )   2715 - 2725   2013.12

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

    Although chromogranin A (CGA) is frequently present in Alzheimer's disease (AD), senile plaques associated with microglial activation, little is known about basic difference between CGA and fibrillar amyloid-β (fAβ) as neuroinflammatory factors. Here we have compared the interleukin-1β (IL-1β) production pathways by CGA and fAβ in microglia. In cultured microglia, production of IL-1β was induced by CGA, but not by fAβ. CGA activated both nuclear factor-κB (NF-κB) and pro-caspase-1, whereas fAβ activated pro-caspase-1 only. For the activation of pro-caspase-1, both CGA and fAβ needed the enzymatic activity of cathepsin B (CatB), but only fAβ required cytosolic leakage of CatB and the NLRP3 inflammasome activation. In contrast, fAβ induced the IL-1β secretion from microglia isolated from the aged mouse brain. In AD brain, highly activated microglia, which showed intense immunoreactivity for CatB and IL-1β, surrounded CGA-positive plaques more frequently than Aβ-positive plaques. These observations indicate differential pathways for the microglial IL-1β production by CGA and fAβ, which may aid in better understanding of the pathological significance of neuroinflammation in AD.

    DOI： 10.1016/j.neurobiolaging.2013.05.018

  • Age-dependent responses of glial cells and leptomeninges during sytemic inflammation. Reviewed International journal

    Wu, Z., Tokuda, Y., Zhang, X-W., Nakanishi, H.

    Neurobiology of Disease   2008.10

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

  • A Mixture of Extracts from Natural Ingredients Reduces the Neurotoxic Polarization of microglia via Modulating NF-κB / NF-E2-related factor 2 Activation Reviewed International journal

    Shuge Gui, Junjun Ni, Shinsuke Mizutani, Norihiro Shigematsu, Hiroshi Nakanishi, Haruhiko Kashiwazaki, Zhou Wu

    Food Science & Nutrition   2024.2

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

    DOI： 10.1002/fsn3.4045

  • Zinc finger protein 335 mediates lipopolysaccharide-induced neurodegeneration and memory loss as a transcriptional factor in microglia Reviewed International journal

    Wei Kong, Zhen Xie, Xiaokang Shang, Yoshinori Hayashi, Fei Lan, Narengaowa, Shuxuan Zhao, Hui Li, Zhenzhen Quan, Zhou Wu, Hiroshi Nakanishi, Hong Qing, Junjun Ni

    Glia   71 ( 12 )   2720 - 2734   2023.11

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

    DOI： 10.1002/glia.24447

  • Critical roles of PU.1/ cathepsin S activation in regulating inflammatory responses of Macrophages in Periodontitis. Reviewed International journal

    Kaige Zhang, Sijian Wang, Zihan Wang, Yiming Jiang, Minghao Huang, Nanqi Liu, Biao Wang, Xin Meng, Zhou Wu, Xu Yan and Xinwen Zhang

    J Periodontal Res.   58 ( 5 )   939 - 947   2023.6

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

    DOI： 10.1111/jre.13153.

  • Microglial Cathepsin E Drives Neuroinflammation and Amyloid β Production in Alzheimer's Disease. Reviewed International journal

    Zhen Xie, Jie Meng, Wei Kong, Zhou Wu, Fei Lan, Narengaowa FNU, Yoshinori Hayashi, Qinghu Yang, Zhantao Bai, Hiroshi Nakanishi, hong qing, and Junjun Ni

    Aging Cell. 21(3) e13565   2022.6

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

    DOI： doi: 10.1111/acel.13565.

  • Differential Expression and Distinct Roles of Proteinase-Activated Receptor 2in Microglia and Neurons in Neonatal Mouse Brain After Hypoxia-Ischemic Injury. Reviewed International journal

    Yicong Liu, Hui Li, Jiangqi Hu, Zhou Wu, Jie Meng, Yoshinori Hayashi, Hiroshi Nakanishi, Hong Qing, Junjun Ni

    Mol Neurobiol.   2021.11

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

    DOI： 10.1007/s12035-021-02594-5.

  • A novel cyclic peptide (Naturido) modulates glia-neuron interactions in vitro and reverses ageing-related deficits in senescence-accelerated mice. Reviewed International journal

    Shinichi Ishiguro*, Tetsuro Shinada*, Zhou Wu*, Mayumi Karimazawa, Michimasa Uchidate, Eiji Nishimura, Yoko Yasuno, Makiko Ebata, Piyamas Sillapakong, Hiromi Ishiguro, Nobuyoshi Ebata, Junjun Ni, Muzhou Jiang, Masanobu Goryo, Keishi Otsu, Hidemitsu Harada, Koichi Suzuki†

    PLoS One   16 ( 1 )   2021.5

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    The use of agents that target both glia and neurons may represent a new strategy for the treatment of ageing disorders. Here, we confirmed the presence of the novel cyclic peptide Naturido that originates from a medicinal fungus (Isaria japonica) grown on domestic silkworm (Bombyx mori). We found that Naturido significantly enhanced astrocyte proliferation and activated the single copy gene encoding the neuropeptide VGF and the neuron-derived NGF gene. The addition of the peptide to the culture medium of primary hippocampal neurons increased dendrite length, dendrite number and axon length. Furthermore, the addition of the peptide to primary microglial cultures shifted CGA-activated microglia towards anti-inflammatory and neuroprotective phenotypes. These findings of in vitro glia–neuron interactions led us to evaluate the effects of oral administration of the peptide on brain function and hair ageing in senescence-accelerated mice (SAMP8). In vivo analyses revealed that spatial learning ability and hair quality were improved in Naturido-treated mice compared with untreated mice, to the same level observed in the normal ageing control (SAMR1). These data suggest that Naturido may be a promising glia–neuron modulator for the treatment of not only senescence, but also Alzheimer’s disease and other neurodegenerative diseases.

    DOI： doi.org/10.1371/journal.pone.0245235

  • The effect of traditional Tibetan guozhuang dance on vascular health in elderly individuals living at high altitudes Reviewed International journal

    Gongfeng L, Aiqin Zhu, Yuling Huang, Jie Meng, Lei Ji, Hongjuan Li, Xiaohong Wang, Junming Luo, Zhou Wu, Shengzheng Wu

    Am J Transl Res.   12 ( 8 )   2020.10

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  • Systemic Exposure to Lipopolysaccharide from Porphyromonas gingivalis Induces Bone Loss-correlated Alzheimer’s Disease-like Pathologies in Middle-aged Mice Reviewed International journal

    Yebo Gu, Zhou Wu, Fan Zeng, Muzhou Jiang, Jessica L. Teeling, Junjun Ni, Ichiro Takahashi.

    J. Alzheimer's Dis.   2020.9

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

    DOI： doi: 10.3233/JAD-200689

  • An impaired intrinsic microglial clock system induces neuroinflammatory alterations in the early stage of amyloid precursor protein knock-in mouse brain Reviewed

    Junjun Ni, Zhou Wu, Jie Meng, Takashi Saito, Takaomi C. Saido, Hong Qing, Hiroshi Nakanishi

    Journal of neuroinflammation   16 ( 1 )   2019.8

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

    DOI： 10.1186/s12974-019-1562-9

  • Cathepsin E in neutrophils contributes to the generation of neuropathic pain in experimental autoimmune encephalomyelitis. Reviewed International journal

    Harada Y, Zhang J, Imari K, Yamasaki R, Ni J, Wu Z, Yamamoto K, Kira JI, Nakanishi H, Hayashi Y

    Pain   2019.4

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  • Induction of bone repair in rat calvarial defects using a combination of hydroxyapatite with phosphatidylserine liposomes Reviewed

    Junko Hatakeyama, Hisashi Anan, Yuji Hatakeyama, Noriyoshi Matsumoto, Fumiko Takayama, Hiro Take, Etsuko Matsuzaki, Masahiko Minakami, Toshio Izumi, Hiroshi Nakanishi

    Journal of Oral Science   61 ( 1 )   111 - 118   2019.1

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    Phosphatidylserine (PS)―normally present on the inner leaflet of the plasma membrane― translocates to the outer leaflet at an early stage of apoptosis. PS-containing liposomes (PSLs) can mimic the effect of apoptotic cells in inducing the secretion of prostaglandin E2 from phagocytes and inhibiting the maturation of dendritic cells and osteoclast precursors. The present study attempted to evaluate the effect of calcium phosphate (in the form of hydroxyapatite [HAP]) in the presence or absence of PSLs for repair of rat calvarial bone defects. The defects, each 5 mm in diameter, were created in the calvaria parietal bone of 8-week-old Wistar rats and subjected to one of the following treatments: no augmentation (Sham), HAP alone, or a mixture of HAP and PSL (HAP+PSL). Micro-computed tomography data showed that the HAP+PSL complexes promoted greater bone regeneration in comparison with either the Sham procedure or HAP alone at 4 and 8 weeks after implantation. The regeneration of calvarial bone defects induced by PSLs was mediated partly through upregulation of the osteogenic marker Alkaline Phosphatase, Type I collagen, osteocalcin, Runx2, and Osterix mRNAs. These data are the first to show that PSLs can influence bone regeneration by regulating osteoblast differentiation.

    DOI： 10.2334/josnusd.17-0488

  • The Critical Role of IL-10 in the Antineuroinflammatory and Antioxidative Effects of Rheum tanguticum on Activated Microglia Invited Reviewed International journal

    Jie Meng, Junjun Ni, Wu Z, Muzhou Jiang, Aiqin Zhu, Hong Qing, and Hiroshi Nakanishi

    OXIDATIVE MEDICINE AND CELLULAR LONGEVITY   2018.9

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

    DOI： 10.1155/2018/1083596

  • Cathepsin H deficiency in mice induces excess Th1 cell activation and early-onset of EAE though impairment of toll-like receptor 3 cascade Reviewed

    Ryo Okada, Xinwen Zhang, Yuka Harada, Hiro Take, Hiroshi Nakanishi

    Inflammation Research   67 ( 5 )   371 - 374   2018.5

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

    Objective: The objective of this study is to investigate the role of cathepsin H (CatH), a lysosomal cysteine protease, in the development of experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis. Methods: EAE was induced in CatH-deficient mice (CatH−/−) and wild-type littermates (+/+) using myelin oligodendrocyte glycoprotein (MOG) 35–55. The effects of CatH deficiency were determined by clinical scoring, mRNA expression levels of Tbx21, Rorc and FoxP3, protein levels of poly(I:C)-induced toll-like receptor 3 (TLR3) and phosphorylation of IRF3, and secretion of interferon-β (IFN-β) by splenocytes. Results and conclusions: CatH−/− showed a significantly earlier disease onset of EAE and increased Th1 cell differentiation in splenocytes. Splenocytes prepared from immunized CatH−/− showed a significant decrease in poly(I:C)-induced increased TLR3 expression, interferon regulatory factor 3 (IRF3) phospholylation and IFN-β secretion. Therefore, CatH deficiency impaired TLR3-mediated activation of IRF3 and consequent secretion of IFN-β from dendritic cells, leading to the enhancement of Th1 cell differentiation and consequent early disease onset of EAE.

    DOI： 10.1007/s00011-018-1136-9

  • Brazilian Green Propolis Prevents Cognitive Decline into Mild Cognitive Impairment in Elderly People Living at High Altitude Invited Reviewed International journal

    Zhu Aiqin *,Wu Z*, Zhong, Xin, Ni, Junjun, Li, Yinglan, Meng, Jie, Du, Can, Zhao Xue, Nakanishi, Hiroshi, Wu Shizheng

    JOURNAL OF ALZHEIMERS DISEASE   63 ( 2 )   551 - 560   2018.3

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

    DOI： 10.3233/JAD-170630

  • Infection of microglia with Porphyromonas gingivalis promotes cell migration and an inflammatory response through the gingipain-mediated activation of protease-activated receptor-2 in mice Reviewed

    Yicong Liu, Hiro Take, Yurika Nakanishi, Junjun Ni, Yoshinori Hayashi, Fumiko Takayama, Yanmin Zhou, Tomoko Kadawaki, Hiroshi Nakanishi

    Scientific Reports   7 ( 1 )   2017.12

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

    DOI： 10.1038/s41598-017-12173-1

  • Dysfunction in diurnal synaptic responses and social behavior abnormalities in cathepsin S-deficient mice Reviewed

    Fumiko Takayama, Xinwen Zhang, Yoshinori Hayashi, Hiro Take, Hiroshi Nakanishi

    Biochemical and Biophysical Research Communications   490 ( 2 )   447 - 452   2017.8

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

    DOI： 10.1016/j.bbrc.2017.06.061

  • Overexpression of Cathepsin E Interferes with Neuronal Differentiation of P19 Embryonal Teratocarcinoma Cells by Degradation of N-cadherin Reviewed

    Yuka Harada, Fumiko Takayama, Kazunari Tanabe, Junjun Ni, Yoshinori Hayashi, Kenji Yamamoto, Hiro Take, Hiroshi Nakanishi

    Cellular and Molecular Neurobiology   37 ( 3 )   437 - 443   2017.4

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    Cathepsin E (CatE), an aspartic protease, has a limited distribution in certain cell types such as gastric cells. CatE is not detectable in the normal brain, whereas it is increasingly expressed in damaged neurons and activated microglia of the pathological brain. Neurons expressing high levels of CatE showed apparent morphological changes, including a marked shrinkage of the cytoplasmic region and beading of neurites, suggesting neuronal damage. The intracellular level of CatE in neurons is strictly regulated at both transcriptional and translational levels. Although the up-regulation of CatE may cause pathological changes in neurons, little information is available about the precise outcome of the increased expression of CatE in neurons. In this study, we have attempted to clarify the outcome of up-regulated CatE gene expression in neurons using the P19 cell neuronal differentiation after the overexpression of CatE. We unexpectedly found that the overexpression of CatE interfered with neuronal differentiation of P19 cells through an impairment of cell aggregate formation. Pepstatin A, an aspartic protease inhibitor, restored the impaired cell aggregation of P19/CatE cells. The small number of P19 cells differentiated into neurons had abnormal morphology characterized by their fusiform cell bodies with short processes. Furthermore, CatE proteolytically cleaved the extracellular domain of N-cadherin. These observations suggest that the overexpression of CatE interferes with neuronal differentiation of P19 cells through an impairment of cell aggregate formation, possibly through proteolytic degradation of N-cadherin.

    DOI： 10.1007/s10571-016-0376-x

  • Boi-ogi-to (TJ-20), a Kampo Formula, Suppresses the Inflammatory Bone Destruction and the Expression of Cytokines in the Synovia of Ankle Joints of Adjuvant Arthritic Rats Reviewed

    Xinwen Zhang, Hiro Take, Yicong Liu, Junjun Ni, Chunfu Deng, Baohong Zhao, Hiroshi Nakanishi, Jing He, Xu Yan

    Evidence-based Complementary and Alternative Medicine   2017   2017.1

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

    DOI： 10.1155/2017/3679295

  • Diurnal dynamic behavior of microglia in response to infected bacteria through the UDP-P2Y 6 receptor system Reviewed

    Fumiko Takayama, Yoshinori Hayashi, Hiro Take, Yicong Liu, Hiroshi Nakanishi

    Scientific Reports   6   2016.7

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

    DOI： 10.1038/srep30006

  • BK channels in microglia are required for morphine-induced hyperalgesia Reviewed

    Yoshinori Hayashi, Saori Morinaga, Jing Zhang, Yasushi Satoh, Andrea L. Meredith, Takahiro Nakata, Hiro Take, Shinichi Kohsaka, Kazuhide Inoue, Hiroshi Nakanishi

    Nature Communications   7   2016.5

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

    DOI： 10.1038/ncomms11697

  • An EP2 Agonist Facilitates NMDA-Induced Outward Currents and Inhibits Dendritic Beading through Activation of BK Channels in Mouse Cortical Neurons Reviewed

    Yoshinori Hayashi, Saori Morinaga, Xia Liu, Jing Zhang, Hiro Take, Takeshi Yokoyama, Hiroshi Nakanishi

    Mediators of Inflammation   2016   2016.1

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

    DOI： 10.1155/2016/5079597

  • Nutrients, Microglia Aging, and Brain Aging Reviewed

    Hiro Take, Janchun Yu, Aiqin Zhu, Hiroshi Nakanishi

    Oxidative Medicine and Cellular Longevity   2016   2016.1

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    As the life expectancy continues to increase, the cognitive decline associated with Alzheimer's disease (AD) becomes a big major issue in the world. After cellular activation upon systemic inflammation, microglia, the resident immune cells in the brain, start to release proinflammatory mediators to trigger neuroinflammation. We have found that chronic systemic inflammatory challenges induce differential age-dependent microglial responses, which are in line with the impairment of learning and memory, even in middle-aged animals. We thus raise the concept of "microglia aging." This concept is based on the fact that microglia are the key contributor to the acceleration of cognitive decline, which is the major sign of brain aging. On the other hand, inflammation induces oxidative stress and DNA damage, which leads to the overproduction of reactive oxygen species by the numerous types of cells, including macrophages and microglia. Oxidative stress-damaged cells successively produce larger amounts of inflammatory mediators to promote microglia aging. Nutrients are necessary for maintaining general health, including the health of brain. The intake of antioxidant nutrients reduces both systemic inflammation and neuroinflammation and thus reduces cognitive decline during aging. We herein review our microglia aging concept and discuss systemic inflammation and microglia aging. We propose that a nutritional approach to controlling microglia aging will open a new window for healthy brain aging.

    DOI： 10.1155/2016/7498528

  • Cathepsin B Regulates Collagen Expression by Fibroblasts via Prolonging TLR2/NF-κB Activation Reviewed

    Xue Li, Hiro Take, Junjun Ni, Yicong Liu, Jie Meng, Weixian Yu, Hiroshi Nakanishi, Yanmin Zhou

    Oxidative Medicine and Cellular Longevity   2016   2016.1

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    Fibroblasts are essential for tissue repair due to producing collagens, and lysosomal proteinase cathepsin B (CatB) is involved in promoting chronic inflammation. We herein report that CatB regulates the expression of collagens III and IV by fibroblasts in response to a TLR2 agonist, lipopolysaccharide from Porphyromonas gingivalis (P.g. LPS). In cultured human BJ fibroblasts, mRNA expression of CatB was significantly increased, while that of collagens III and IV was significantly decreased at 24 h after challenge with P.g. LPS (1 μg/mL). The P.g. LPS-decreased collagen expression was completely inhibited by CA-074Me, the specific inhibitor of CatB. Surprisingly, expression of collagens III and IV was significantly increased in the primary fibroblasts from CatB-deficient mice after challenge with P.g. LPS. The increase of CatB was accompanied with an increase of 8-hydroxy-2′-deoxyguanosine (8-OHdG) and a decrease of IκBα. Furthermore, the P.g. LPS-increased 8-OHdG and decreased IκBα were restored by CA-074Me. Moreover, 87% of CatB and 86% of 8-OHdG were colocalized with gingival fibroblasts of chronic periodontitis patients. The findings indicate the critical role of CatB in regulating the expression of collagens III and IV by fibroblasts via prolonging TLR2/NF-κB activation and oxidative stress. CatB-specific inhibitors may therefore improve chronic inflammation-delayed tissue repair.

    DOI： 10.1155/2016/7894247

  • Nutrients, Microglia Aging, and Brain Aging Reviewed

    Hiro Take, Janchun Yu, Aiqin Zhu, Hiroshi Nakanishi

    Oxidative Medicine and Cellular Longevity   2016   2016.1

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

    DOI： 10.1155/2016/7498528

  • Cathepsin B Regulates Collagen Expression by Fibroblasts via Prolonging TLR2/NF-κB Activation Reviewed

    Xue Li, Hiro Take, Junjun Ni, Yicong Liu, Jie Meng, Weixian Yu, Hiroshi Nakanishi, Yanmin Zhou

    Oxidative Medicine and Cellular Longevity   2016   2016.1

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

    DOI： 10.1155/2016/7894247

  • The critical role of proteolytic relay through cathepsins B and E in the phenotypic change of microglia/macrophage Reviewed International journal

    NI JUNJUN, Wu Z, Christoph Peterts, Kenji, Yamamoto, Hong Qin, Hiroshi Nakanishi

    Journal of Neuroscience   35   12488 - 501   2015.9

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

    DOI： 10.1523/JNEUROSCI.1599-15.2015

  • Lessons from Microglia Aging for the Link between Inflammatory Bone Disorders and Alzheimer’s Disease, Reviewed International journal

    Wu Z, Hiroshi Nakanishi

    Journal of Immunology Research   Volume 2015 (2015),   1 - 10   2015.3

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  • The Neuroprotective Effects of Ratanasampil on Oxidative Stress-Mediated Neuronal Damage in Human Neuronal SH-SY5Y Cells Reviewed International journal

    Aiqin Zhu, Wu Z, Jie Meng, Patrick L. McGeer, Yi Zhu, Hiroshi Nakanishi, Shizheng Wu

    Oxidative Medicine and Cellular Longevity   Volume 2015 (2015),   1 - 9   2015.3

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  • Lessons from Microglia Aging for the Link between Inflammatory Bone Disorders and Alzheimer's Disease Reviewed

    Zhou Wu, Hiroshi Nakanishi

    Journal of Immunology Research   2015   2015.1

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    Bone is sensitive to overactive immune responses, which initiate the onset of inflammatory bone disorders, such as rheumatoid arthritis and periodontitis, resulting in a significant systemic inflammatory response. On the other hand, neuroinflammation is strongly implicated in Alzheimer's disease (AD), which can be enhanced by systemic inflammation, such as that due to cardiovascular disease and diabetes. There is growing clinical evidence supporting the concept that rheumatoid arthritis and periodontitis are positively linked to AD, suggesting that inflammatory bone disorders are risk factors for this condition. Recent studies have suggested that leptomeningeal cells play an important role in transducing systemic inflammatory signals to brain-resident microglia. More importantly, senescent-type, but not juvenile-type, microglia provoke neuroinflammation in response to systemic inflammation. Because the prevalence of rheumatoid arthritis and periodontitis increases with age, inflammatory bone disorders may be significant sources of covert systemic inflammation among elderly people. The present review article highlights our current understanding of the link between inflammatory bone disorders and AD with a special focus on microglia aging.

    DOI： 10.1155/2015/471342

  • The Neuroprotective Effects of Ratanasampil on Oxidative Stress-Mediated Neuronal Damage in Human Neuronal SH-SY5Y Cells Reviewed

    Aiqin Zhu, Hiro Take, Jie Meng, Patrick L. McGeer, Yi Zhu, Hiroshi Nakanishi, Shizheng Wu

    Oxidative Medicine and Cellular Longevity   2015   2015.1

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    DOI： 10.1155/2015/792342

  • The downward spiral of periodontitis and diabetes in Alzheimer's disease Extending healthy life expectancy through oral health Reviewed

    Hiroshi Nakanishi, Hiro Take

    Journal of Oral Biosciences   57 ( 3 )   139 - 142   2015.1

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

    DOI： 10.1016/j.job.2015.05.002

  • The Neuroprotective Effects of Ratanasampil on Oxidative Stress-Mediated Neuronal Damage in Human Neuronal SH-SY5Y Cells Reviewed

    Aiqin Zhu, Hiro Take, Jie Meng, Patrick L. McGeer, Yi Zhu, Hiroshi Nakanishi, Shizheng Wu

    Oxidative Medicine and Cellular Longevity   2015   2015.1

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

    DOI： 10.1155/2015/792342

  • Connection between periodontitis and Alzheimer's disease: possible roles of microglia and leptomeningeal cells Reviewed International journal

    Wu Z, Hiroshi Nakanishi

    Journal of Pharmacological Sciences,   126 ( 1 )   8 - 13   2014.12

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

    DOI： 10.1254/jphs.14 R11CP

  • Cathepsin D deficiency induces oxidative damage in brain pericytes and impairs the blood-brain barrier Reviewed International journal

    Okada Ryo, Wu Z, junjun Ni, J Zhang, Yoshito Yoshimine, Christoph Peters, Paul Saftig, Hiroshi Nakanishi

    Molecular and Cellular Neuroscience   64   51 - 60   2014.12

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

    DOI： 10.1016/j.mcn.2014.12.002

  • “Autophagy in superficial spinal dorsal horn accelerates the cathepsin B-dependent morphine antinociceptive tolerance” Reviewed International journal

    Yoshinori Hayashi, yuka Koga, Xinwen Zhang, Christoph Peters, Yanagawa Y, Wu Z, Takeshi Yokoyama, Hiroshi Nakanishi

    Neuroscience,   275   384 - 394   2014.5

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

    DOI： 10.1016/j.neuroscience.2014.06.037

  • Peripheral role of cathepsin S in Th1 cell-dependent transition of nerve injury-induced acute pain to a chronic pain state. Reviewed International journal

    Zhang XW, Wu Z, Yoshinori Hayashi, Okada Ryo, Hiroshi Nakanishi

    J Neurosci.   2014.2

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    DOI： 10.1523/JNEUROSCI.3681-13.2014

  • The intrinsic microglial molecular clock controls synaptic strength via the circadian expression of cathepsin S Reviewed

    Yoshinori Hayashi, Koyanagi Satoru, Naoki Kusunose, Ryo Okada, Hiro Take, Hidetoshi Saitoh, Kiyoharu Ukai, Shinichi Kohsaka, Kazuhide Inoue, Shigehiro Ohdo, Hiroshi Nakanishi

    Scientific Reports   3   2013.10

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

    DOI： 10.1038/srep02744

  • Brazilian green propolis suppresses the hypoxia-induced neuroinflammatory responses by inhibiting NF-κB activation in microglia. Reviewed International journal

    Wu Z, Zhu A, Takayama F, Okada Ryo, Liu Y, Yoshinori Hayashi, Wu S, Hiroshi Nakanishi

    Oxid Med Cell Longev   2013.9

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    DOI： 10.1155/2013/906726

  • Possible involvement of aiPLA2 in the phosphatidylserine-containing liposomes induced production of PGE2 and PGD2 in microglia. Reviewed International journal

    Ｔａｋａｙａｍａ　Ｆ, Wu Z, Ｍａ　ＨＭ, Okada Ryo, Yoshinori Hayashi, Hiroshi Nakanishi

    J Neuroimmunol.   2013.9

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

    DOI： 10.1016/j.jneuroim.2013.06.011.

  • Age-dependent neuroinflammatory responses and deficits in long-term potentiation in the hippocampus during systemic inflammation. Reviewed International journal

    Lui X, Wu Z, Yoshinori Hayashi, Hiroshi Nakanishi

    Neuroscience.   2012.8

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

    DOI： 10.1016/j.neuroscience.2012.04.050.

  • Microglial cathepsin B contributes to the initiation of peripheral inflammation-induced chronic pain. Reviewed International journal

    Ｓｕｎ　Ｌｉ, Wu Z, Yoshinori Hayashi, Peter C, TSUDA MAKOTO, Kazuhide Inoue, Hiroshi Nakanishi

    J Neurosci   2012.8

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  • Phosphatidylserine-containing liposomes: potential pharmacological interventions against inflammatory and immune diseases through the production of prostaglandin E(2) after uptake by myeloid derived phagocytes. Reviewed International journal

    Ma HM, Wu Z, Nakanishi H.

    Lab Invest.   91 ( 6 )   2011.1

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  • Acute p38-mediated inhibition of NMDA-induced outward currents in hippocampal CA1 neurons by interleukin-1beta. Reviewed International journal

    Zhang R, Sun L, Yoshinori Hayashi, Liu X, Koyama S, Wu Z, Hiroshi Nakanishi

    Neurobiol Dis   2010.8

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

    DOI： 10.1016/j.nbd.2009.12.028

  • Cathepsin B-dependent motor neuron death after nerve injury in the adult mouse Reviewed International journal

    Sun L, Wu Z, Baba M, Peters C, Uchiyama Y, Nakanishi H.

    Biochem Biophys Res Commun   399 ( 3 )   2010.8

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  • Phosphatidylserine-containing liposomes inhibit the differentiation of osteoclasts and trabecular bone loss Reviewed International journal

    Wu Z, Ma HM, Kukita T, Nakanishi Y, Nakanishi H.

    J Immunol.   184 ( 6 )   2010.5

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    Publishing type：Research paper (scientific journal)  

    本論文は細胞膜りン脂質であるスファチジルセリン(PS)含有リポソーム破骨細胞の成熟を抑制することと慢性関節リウマチの動物モデルであるラットアジュバント関節炎に伴う距腿関節における骨破壊を抑制することを発現した。その機序としてPSリポソームは破骨前駆細胞に取り込まれTGF-beta1とPGE2の産生分泌を誘導し、RANKL、RANKの発現ならびに破骨前駆細胞におけるICAM-１、CD44などの融合因子の発現を抑制することで破骨細胞の成熟ならびに骨破壊を強力に抑制することが明らかになった。これらの知見はPSリポソームが慢性関節リウマチ、歯周炎ならびに骨粗鬆症に伴う骨破壊に対する効果的かつ安全な治療薬になり得ると考えている。

  • Involvement of cathepsin B in the processing and secretion of interleukin-1beta in chromogranin A-stimulated microglia. Reviewed International journal

    Terada K, Yamada J, Hayashi Y, Wu Z, Uchiyama Y, Peters C, Nakanishi H

    Glia.   2010.1

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  • A possible suppressive role of galectin-3 in upregulated osteoclastogenesis accompanying adjuvant-induced arthritis in rats. Reviewed International journal

    Li Y. J., Kukita A., Teramachi J., Nagata K., Wu Z., Akamine A., and Kukita T.

    Lab. Invest.   2009.5

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  • Possible involvement of cathepsin B released by microglia in methylmercury-induced cerebellar pathological changes in the adult rats Reviewed International journal

    Sakamoto M., Miyamoto K. I., Wu Z., and Nakanishi H.

    Neurosci. Lett   2008.9

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  • Reverse of brain aging by an overexpression of human mitochondrial transcription factor A in mice. Reviewed International journal

    Hayashi Y., Yoshida M., Yamato M., Ide T., Wu Z., Ochi-Shindou M., Kanki T., Kang D., Sunagawa K., Tsutsui H., and Nakanishi H.

    J. Neurosci   2008.5

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  • Inhibition of NMDA-induced outward currents by interleukin-1beta in hippocampal neurons. International journal

    Zhang R., Yamada J., Hayashi Y., Wu Z., Koyama S., Nakanishi H.

    Biochem. Biophys. Res. Commun   2008.5

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  • Reduced synaptic acticity precedes synaptic stripping in vagal motoneurons after axotomy Reviewed International journal

    Yamada J., Hayashi Y., Jinno S., Wu Z., Inoue K., Kohsaka S., Nakanishi H

    Glia   2007.9

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  • Involvement of lysosomal storage-induced p38 MAP kinase activation in the overproduction of nitric oxide by microglia in cathepsin D- deficient mice Reviewed International journal

    Yamasaki R., Zhang J., Koshiishi I., Sastradipura Suniarti D.F.,Wu Z., Peters C., Schwake M., UchiyamaY., Kira J. I., Saftig P., Utsumi H., and Nakanishi H

    Mol. Cell. Neurosci.   2007.7

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  • Involvement of Prostaglandin E2 Released from Leptomeningeal Cells in Increased Expression of TGF-beta1 in Glial Cells and Cortical Neurons during Systemic Inflammation. Reviewed International journal

    Wu Z, Hayashi Y, Jian Zhang, Nakanishi H.

    J Neurosci Res.   2007.1

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  • The intra-arterial injection of microglia protects hippocampal CA1 neurons against global ischemia-induced functional deficits in rats Reviewed

    Yoshinori Hayashi, Y. Tomimatsu, H. Suzuki, Jun Yamada, Hiro Take, H. Yao, Y. Kagamiishi, N. Tateishi, M. Sawada, Hiroshi Nakanishi

    Neuroscience   142 ( 1 )   87 - 96   2006.9

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    In the present study, we have attempted to elucidate the effects of the intra-arterial injection of microglia on the global ischemia-induced functional and morphological deficits of hippocampal CA1 neurons. When PKH26-labeled immortalized microglial cells, GMIR1, were injected into the subclavian artery, these exogenous microglia were found to accumulate in the hippocampus at 24 h after ischemia. In hippocampal slices prepared from medium-injected rats subjected to ischemia 48 h earlier, synaptic dysfunctions including a significant reduction of synaptic responses and a marked reduction of long-term potentiation (LTP) of the CA3-CA1 Schaffer collateral synapses were observed. At this stage, however, neither significant neuronal degeneration nor gliosis was observed in the hippocampus. At 96 h after ischemia, there was a total loss of the synaptic activity and a marked neuronal death in the CA1 subfield. In contrast, the basal synaptic transmission and LTP of the CA3-CA1 synapses were well preserved after ischemia in the slices prepared from the microglia-injected animals. We also found the microglial-conditioned medium (MCM) to significantly increase the frequency of the spontaneous postsynaptic currents of CA1 neurons without affecting the amplitude, thus indicating that MCM increased the provability of the neurotransmitter release. The protective effect of the intra-arterial injected microglia against the ischemia-induced neuronal degeneration in the hippocampus was substantiated by immunohistochemical and immunoblot analyses. Furthermore, the arterial-injected microglia prevented the ischemia-induced decline of the brain-derived neurotrophic factor (BDNF) levels in CA1 neurons. These observations strongly suggest that the arterial-injection of microglia protected CA1 neurons against the ischemia-induced neuronal degeneration. The restoration of the ischemia-induced synaptic deficits and the resultant reduction of the BDNF levels in CA1 neurons, possibly by the release of diffusible factor(s), might thus contribute to the protective effect of the arterial-injection of microglia against ischemia-induced neuronal degeneration.

    DOI： 10.1016/j.neuroscience.2006.06.003

  • The intra-arterial injection of microglia protects hippocampal CA1 neurons against global ischemia-induced functional deficits in rats. Reviewed International journal

    Hayashi Y, Tomimatsu Y, Suzuki H, Yamada J, Wu Z, Yao H, Kagamiishi Y, Tateishi N, Sawada M, Nakanishi H.

    Neuroscience   2006.4

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  • Involvement of COX-1 and up-regulated prostaglandin e synthases in phosphatidylserine liposome-induced prostaglandin E2 production by microglia Reviewed

    Jian Zhang, Shunsuke Fujii, Zhou Wu, Sadayuki Hashioka, Yoshitaka Tanaka, Akiko Shiratsuchi, Yoshinobu Nakanishi, Hiroshi Nakanishi

    Journal of Neuroimmunology   172 ( 1-2 )   112 - 120   2006.3

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

    DOI： 10.1016/j.jneuroim.2005.11.008

  • Involvement of COX-1 and up-regulated prostaglandin E synthases in phosphatidylserine　liposome-induced prostaglandin E2 production by microglia. Reviewed International journal

    Zhang J, Fujii S, Wu Z, Hashioka S, Tanaka Y, Shiratsuchi A, Nakanishi Y, Nakanishi H.

    J Neuroimmunol.   2006.1

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  • Inhibition of histone deacetylase suppresses osteoclastogenesis and bone destruction by inducing IFN-β production Reviewed

    Takahiro Nakamura, Toshio Kukita, Takeo Shobuike, Kengo Nagata, Hiro Take, Kenji Ogawa, Takao Hotokebuchi, Osamu Kohashi, Akiko Kukita

    Journal of Immunology   175 ( 9 )   5809 - 5816   2005.11

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  • Leptomeningeal cells activate microglia and astrocytes to induce IL-10 production by releasing pro-inflammatory cytokines during systemic inflammation. Reviewed International journal

    Wu Z, Zhang J, Nakanishi H.

    J Neuroimmunol.   167 ( 1-2 )   90 - 98   2005.9

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

    DOI： 10.1016/j.jneuroim.2005.06.025

  • Inhibition of Histone Deacetylase Suppresses Osteoclastogenesis and Bone Destruction by Inducing IFN-{beta} Production. Reviewed International journal

    Nakamura T, Kukita T, hobuike T, Nagata K, Wu Z, Ogawa K, Hotokebuchi T, Kohashi O, Kukita A.

    J Immunol.   175 ( 9 )   5809 - 5816   2005.7

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  • Regulation of osteoclastogenesis by Simon extracts composed of caffeic acid and related compounds: successful suppression of bone destruction accompanied with adjuvant-induced arthritis in rats. Reviewed International journal

    Tang QY, Kukita T, Ushijima Y, Kukita A, Nagata K, Sandra F, Watanabe T, Toh K, Okuma Y, Kawasaki S, Rasubala L, Teramachi J, Miyamoto I, Wu Z, Iijima T.

    Histochem Cell Biol   125 ( 3 )   215 - 225   2005.2

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

    DOI： 10.1007/s00418-005-0062-4

  • Possible involvement of MIP-1alpha in the recruitment of osteoclast progenitors to the distal tibia in rats with adjuvant-induced arthritis Reviewed International journal

    Toh K, Kukita T, Wu Z, Kukita A, Sandra F, Tang QY, Nomiyama H, Iijima T.

    Lab Invest.   84 ( 9 )   1092 - 1102   2004.9

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

    DOI： 10.1038/labinvest.3700132

  • Effect of the resection of the sciatic nerve on the Th1/Th2 balance in the synovia of the ankle joint of adjuvant arthritic rats. Reviewed International journal

    Wu Z, Toh K, Nagata K, Kukita T, Iijima T.

    Histochem Cell Biol.   121 ( 2 )   141 - 147   2004.1

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

    DOI： 10.1007/s00418-003-0614-4

  • Involvement of sensory nerves and immune cells in osteophyte formation in the ankle joint of adjuvant arthritic rats Reviewed

    Wu Z, Kengo Nagata, Tadahiko Iijima

    Histochemistry and Cell Biology   118 ( 3 )   213 - 220   2002.10

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  • Involvement of sensory nerves and immune cells in osteophyte formation in the ankle joint of adjuvant arthritic rats. Reviewed International journal

    Wu Z, Nagata K, Iijima T.

    Histochem Cell Biol.   118 ( 3 )   213 - 220   2002.5

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

    DOI： 10.1007/s00418-002-0443-x

  • Immunohistochemical study of NGF and it receptors in the synovial membrane of the ankle joint of adjuvant-induced arthritic rats. Reviewed International journal

    Wu Z, Nagata K, Iijima T.

    Histochem Cell Biol.   114 ( 6 )   453 - 459   2000.12

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Books

  • ≪ヒト常在菌叢と生理機能・全身疾患≫ （監修者　落合邦康）

    武　洲（Role：Joint author）

    ジーエムジー出版、東京、日本  2020.8 

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    Responsible for pages：pp. 257-265.   Language：Others   Book type：Scholarly book

  • 歯周病によるアリツハイマ―病の関与メカニズム　≪アリツハイマ―病－発症メカニズムと新規診断法・創薬・治療開発

    武　洲（Role：Sole author）

    エヌ・ティ－エス株式会社、東京、日本  2018.6 

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    Responsible for pages：pp. 40-44   Language：Japanese   Book type：Scholarly book

  • Microglia-aging and pain: Microglial cathepsin B-dependent IL-1 production, In: Interleukin-1: Genetics, Inflammatory Mechanisms and Role in Disease

    Nakanishi H, Wu Z（Role：Joint author）

    Nova Science Publishers  2013.6 

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    Responsible for pages：pp. 143-156   Language：English   Book type：General book, introductory book for general audience

  • TNF-a signaling and cathepsin B, In: Tumor Necrosis Factor: Structure. Enzyme Regulation and Role in Health and Disease

    Wu Z, Nakanishi H（Role：Joint author）

    Nova Science Publisher Inc  2013.6 

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    Responsible for pages：pp. 113-128   Language：English   Book type：General book, introductory book for general audience

  • Neuroimmunology Research Focus Chapter 4 Age-Dependent Differential Activation Profiles of Glial Cell by the Leptomeninges During Systemic Inflammation

    Zhou Wu and Hiroshi Nakanishi（Role：Joint author）

    Nova Science Pulishers, Inc.  2007.9 

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    Responsible for pages：pp. 101-118.   Language：English   Book type：Scholarly book

  • Common Pathways Linking Neurodegenerative Diseases – The Role of Inflammation. ebook

    Ni J, Wu Z（Role：Joint author）

    Frontiers in Cellular Neuroscience  2021.11 

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    Responsible for pages：pp. 140-152.   Language：English   Book type：Scholarly book

  • Osteoclasts Morphology, Fuctions and Clinical Immplications (ediators: Alexander J Brown and Johanna S Walker )

    Wu Z, Hiroshi Nakanishi（Role：Joint author）

    Nova Science Publisher, Inc., New York  2012.12 

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    Responsible for pages：chaper 7, Multiple Functions of Osteoclasts and Potential Usefulness of Phosphatidylserine-Containing Liposomes on Bone Diseases 131-140   Language：English   Book type：Scholarly book

  • Cathepsin-dependent neuronal death pathways induced by methylmercury、Methylmercury: Formation, Sources and Health Effects (Ed: Andrew P. Clampet)

    Wu Z, Hiroshi Nakanishi（Role：Joint author）

    Nova Science Publisher, Inc., New York  2011.4 

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    Language：English   Book type：Scholarly book

  • chapter 5 Regulation of Myeloid Derived Phagocytes by Phosphatidylserine-Containing Liposomes: Possible Involvement of Prostaglandin E2 and the Potential Therapeutic Usefulness Prostaglandins: Biochemistry, Function, Types and Roles

    Zhou Wu and Hiroshi Nakanishi（Role：Joint author）

    Nova Science Publishers, Inc., New York  2010.9 

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    Responsible for pages：pp.81-92   Language：English   Book type：Scholarly book

  • Nakanishi,Regulation of myeloid derived phagocytes by phosphatidylserine-containing liposomes: Possible involvement of prostaglandid E2 and the potential terapeutic application,,Prostaglandins: Biochemistry, Functions, Types and Roles (Ed., Gillian M. Goodwin)

    Hiro Take, Hiroshi Nakanishi（Role：Joint author）

    Nova Science Publisher, Inc., New York  2010.4 

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    Responsible for pages：pp81-92.   Language：English   Book type：General book, introductory book for general audience

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Presentations

  • 口腔から認知症予防策を考える Invited

    武　洲

    第38回保団連シンポジウム  2023.10 

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    Event date： 2023.10 - 2024.10

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：東京   Country：Japan  

    世界一の長寿国であるわが国では、高齢の認知症患者数が増加し続けている。2025年には高齢者の5人に1人、国民の17人に1人が認知症になると予測されている。認知症の 7 割を占めるアルツハイマー型認知症（Alzheimer's disease, AD）の 9 割は加齢に伴い発症し、20数年の長いスパンで進行する。一方、中高年者では口腔感染症である歯周病の有病率が6割を超え、加齢に連れ、症状が進行した人の割合も増える。AD患者に歯周病有病率が高い診療現場から「歯周病はADのリスクファクター」という仮説が提唱され、多くの臨床エビデンスにより支持されている。　さらに歯周病病原菌であるP.gingivalis 菌成分であるP.gingivalis LPSやgingipainがADの剖検脳に検出され、ADに歯周病の関与メカニズム解明が注目されるようになった。
    AD脳病態の特徴として、アミロイド(A)の蓄積と形成される老人斑とタウの過剰リン酸化による神経原線維変化があるが、ミクログリアに依存する脳内炎症がAの蓄積、タウの過剰リン酸化を促進する。一方、全身炎症がミクログリアを活性化させ脳内炎症を誘発し慢性化させている。私たちは歯周病を慢性炎症と捉え、P.gingivalis菌とその成分のAD への関与メカニズムを解明し、日本からこのメカニズムを発信し続けている。これまでP.gingivalis菌とその成分が　１）AD 脳病態を誘発し促進する　２）全身炎症を増大させる　３）全身でA産生を誘導する　４）全身のを脳内輸入させるように、多方向的にADの誘発と進行に関わることが明らかになっている。本シンポジウムでは.gingivalis菌のADへの関与について、私たちが得られた知見を踏まえて解説するとともに、全身炎症の介入することにより、認知機能の改善効果も紹介する。
    2019（令和元）年6月に策定された「認知症施策推進大綱」に、「共生」と「予防」を車の両輪として、この施策を推進すると公表しており、その「予防」を「認知症にならない」ではなく、「認知症になるのを遅らせる」、「認知症になっても進行を緩やかにする」と定義し、具体的に70 歳代での発症を 10 年間で１歳遅らせることを目標と挙げている。ADが発症してから根本的な治療法がない現状の中、治療と予防の可能な口腔感染症ならびに全身炎症を減らすことが、ADの発症と進行を遅らせる認知症予防対策として提案したい。

  • 口腔から考える認知症予防 Invited

    武　洲

    第23回日本抗加齢医学会総会  2023.6 

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    Event date： 2023.6

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：東京   Country：Japan  

    地球規模の高齢人口増加に伴い、世界の認知症患者は 2050年には1 億 3千万人を突破すると推計されている。高齢化率世界一の我が国では2025年には高齢者の3人に1人が認知症とその予備軍になると見込まれる「2025年問題」に直面している。認知症の 7 割を占めるアルツハイマー型認知症（Alzheimer's disease, AD）の 9 割は加齢に伴い発症し、ADの脳病態にはアミロイドβ蓄積による老人班、Tau蛋白質過剰リン酸化による神経原線維変性ならびにミクログリア活性化に伴う脳内炎症がある。
    糖尿病やリウマチ関節炎など全身炎症性疾患はADの発症と病態進行に関与し、口腔慢性炎症の歯周病は糖尿病やリウマチ関節炎を促す。一方、歯周病は高齢者ならびにAD患者における認知機能低下と正相関し、歯周病病原菌のP.gingvalis菌に由来するlipopolysaccharide（P.gLPS）などの成分がAD剖検脳にも検出されていることから、口腔と認知症への関与が注目されている。私たちは長年にわたり炎症のADへ関与するメカニズムを追究し続けて明らかにしたADの誘発と増悪因子を対象にした認知症予防開発も行っている。
    ADは20数年の長いスパンで進行するが、私たちはこれまでP.gingvalis菌が年齢に依存した １）AD脳病態を誘発し促進すること、２）全身炎症を増大させること、３）脳外でアミロイドβ産生を誘導すること、４）脳外アミロイドβを脳内に輸入させることを明らかにしてきた。本シンポジウムでは口腔から多方向にADの発症と進行に関与するメカニズムを解説し、炎症を対象とした認知症の予防開発も紹介する。
    炎症は細胞レベルの老化を促進する観点から、口腔より「炎症軽減」することで細胞レベル抗老化効果を得ることができる。抗加齢的な視点から、口腔より「炎症制御」をすることで加齢につれて増加する認知症の発症と進行を遅らせる現実的な予防アプローチとして提案したい。

  • 認知症を口から防ぐ〜口腔ブレインサイエンス〜 Invited International conference

    武　洲

    国際医科学研究会 第20回フォーラム  2022.6 

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    Event date： 2022.6

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

    Country：Japan  

  • 口腔感染症と認知症：関連メカニズムから予防策を考える Invited

    武　洲

    第30回日本病態生理学会大会  2022.1 

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    Event date： 2022.1 - 2022.6

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

    Venue：福岡   Country：Japan  

  • 歯周病がアルツハイマー型認知症に関与するメカニズム Invited

    武　洲

    認知症と口腔機能研究会 JRSDOF 第２回学術集会  2021.8 

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    Event date： 2021.8

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

    Venue：オンライン開催   Country：Japan  

  • The involvement mechanism of P. gingivalis infection in Alzheimer disease Invited International conference

    Zhou WU

    SNU – KYUSHU JOINT SYMPOSIUM  2021.6 

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    Event date： 2021.6

    Language：Others   Presentation type：Oral presentation (general)  

    Venue：オンライン開催   Country：Japan  

  • 全身炎症によるミクログリア活性化とアルツハイマー病 Invited

    武　洲

    116回日本精神神経学会学術総会  2020.9 

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    Event date： 2020.9

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

    Venue：オンライン開催   Country：Japan  

  • 口腔からアルツハイマー型認知症を考える Invited

    武　洲

    第42回九州口腔衛生学会総会  2020.9 

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    Event date： 2020.9

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

    Venue：オンライン開催   Country：Japan  

  • Chronic systemic exposure of Lipopolysaccharide from Porphyromonas gingivalis induces memory decline through the upregulation of the bone loss promotion molecule IL-17 in middle-aged mice

    Yebo Gu, Junjun Ni, Zhou Wu, Ichiro Takahashi

    第72回日本薬理学会西南部会  2019.11 

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    Event date： 2019.11

    Language：English   Presentation type：Oral presentation (general)  

    Venue：Naha   Country：Japan  

  • Chronic systemic exposure of PgLPS induces long bone loss and cognitive decline in middle-aged mice

    Yebo Gu, Junjun Ni, Zhou Wu, Ichiro Takahashi

    第78回日本矯正歯科学会  2019.11 

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    Event date： 2019.11

    Language：English   Presentation type：Oral presentation (general)  

    Venue：長崎   Country：Japan  

  • Chronic systemic exposure of Lipopolysaccharide from Porphyromonas gingivalis induces Memory decline and Bone loss in Middle-aged Mice International conference

    Yebo Gu, Junjun Ni, Muzhou Jiang, Zhou Wu, Ichiro Takahashi

    6th Congress of ASCNP  2019.10 

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    Event date： 2019.10

    Language：English   Presentation type：Oral presentation (general)  

    Venue：Fukuoka   Country：Japan  

  • Microglia induces tau hyperphosphorylation of cultured neurons after exposure to Porphyromonas gingivalis LPS International conference

    Muzhou Jiang, Junjun Ni, Yebo Gu, Zhou Wu

    6th Congress of ASCNP  2019.10 

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    Event date： 2019.10

    Language：English   Presentation type：Oral presentation (general)  

    Venue：Fukuoka   Country：Japan  

  • Porphyromonas gingivalis infected Leptomeningeal Cells Reduces Synapses Proteins in Primary Cultured Neurons International conference

    Wanyi Huang, Junjun Ni, Zhou Wu,

    6th Congress of AsCNP  2019.10 

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    Event date： 2019.10

    Language：English   Presentation type：Oral presentation (general)  

    Venue：Fukuoka   Country：Japan  

  • Porphyromonas gingivalis infection increases RAGE production in hCMEC/D3 cell line International conference

    Fan Zeng, Junjun Ni, Zhou Wu

    6th Congress of ASCNP  2019.10 

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    Event date： 2019.10

    Language：English   Presentation type：Oral presentation (general)  

    Venue：Fukuoka   Country：Japan  

  • Inflammation and Lysosomal Enzymes: Prevention Approach of Cognitive Decline Invited International conference

    Zhou WU

    Neurology Conference  2019.6 

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    Event date： 2019.6

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

    Venue：Tokyo   Country：Japan  

  • ブラジル産グリーンプロポリスは、チベット高原に住む高齢者の全身炎症を軽減して認知機能の低下を防ぐ

    Zhu A, Ni J, Meng J, Nakanishi H ,Wu Z

    第60回歯科基礎医学会学術大会  2018.9 

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    Event date： 2019.6

    Language：Japanese  

    Venue：福岡   Country：Japan  

  • チベット薬Ratanasampilは、低酸素によるミクログリアにおける酸化ストレスならびにNF-κB活性化に依存した炎症反応を抑制する

    Jie Meng, Junjun Ni, Yoshinori Hayashi, Hiroshi Nakanishi, Aiqin Zhu　and Zhou Wu

    第60回歯科基礎医学会学術大会  2018.9 

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    Event date： 2019.6

    Language：Japanese  

    Venue：福岡   Country：Japan  

  • Porphyromonas gingivalis由来LPSの慢性投与は中年モウスにおける骨量低下ならびに記憶低下を誘発する

    Yebo Gu, Junjun Ni, Zhou Wu, Ichiro Takahashi

    第60回歯科基礎医学会学術大会  2018.9 

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    Event date： 2019.6

    Language：Japanese  

    Venue：福岡   Country：Japan  

  • 慢性全身性Porphyromonas gingivalis感染に伴う全身性アミロイドβ代謝におけるマクロファージの関与

    Ran Nie, Junjun Ni, Yoshinori Hayashi, Zhou Wu, Yanmin Zhou

    第60回歯科基礎医学会学術大会  2018.9 

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    Event date： 2019.6

    Language：Japanese  

    Venue：福岡   Country：Japan  

  • ジンジバリス菌とアルツハイマー病 Invited

    武　洲

    第60回歯科基礎医学会学術大会  2018.9 

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    Event date： 2019.6

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

    Venue：福岡   Country：Japan  

  • ジンジバリス菌とアルツハイマー病 Invited

    武　洲

    「Hindgut Club Japan」シンポジウム  2018.12 

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    Event date： 2019.6

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

    Venue：東京   Country：Japan  

  • ブラジル産プロポリスは低酸素によるミクログリア依存性脳炎症反応を抑制する

    姜慕舟，倪軍軍，武洲

    第92回日本薬理学会年会  2019.3 

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    Event date： 2019.6

    Language：Japanese  

    Venue：大阪   Country：Japan  

  • 酸化ストレス誘発されるニューロン障害およびミクログリア依存性脳炎症に対するRatanasampilの抑制作用

    孟　ジエ, 朱　愛琴，倪　軍軍，林　良憲，中西　博，武　洲

    第92回日本薬理学会年会  2019.3 

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    Event date： 2019.6

    Language：Japanese  

    Venue：大阪   Country：Japan  

  • Porphyromonas gingivalis感染による内皮細胞におけるRAGE発現が増加させる

    曽　凡, 倪　軍軍，武　洲

    第92回日本薬理学会年会  2019.3 

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    Event date： 2019.6

    Language：Japanese  

    Venue：大阪   Country：Japan  

  • Porphyromonas gingivalis由来LPSによる中年マウスおける記憶低下ならびに骨量減少の誘発

    顧也博，倪軍軍，姜慕舟，武洲，高橋一郎

    第92回日本薬理学会年会  2019.3 

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    Event date： 2019.6

    Language：Japanese  

    Venue：大阪   Country：Japan  

  • The transduce effect of leptomeningeal cells in peripheral exposure of Porphyromonas gingivalis induced neurodegeneration in Alzheimer’s disease.

    黄婉怡,　倪軍軍，武洲

    第92回日本薬理学会年会  2019.3 

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    Event date： 2019.6

    Language：Japanese  

    Venue：Osaka   Country：Japan  

  • Cathepsin B, novel therapeutic target for microglia-mediated neuroinflammation Invited International conference

    Wu Z

    special seminar in University of Southampton  2017.2 

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    Event date： 2018.6

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

    Venue：University of Southampton   Country：United Kingdom  

  • 歯周病菌感染による脳内アルツハイマー様病態の誘発メカニズム Invited

    武　洲

    第58回歯科基礎医学会学術大会・サテライトシンポジウム  2016.8 

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    Event date： 2018.6

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

    Venue：札幌   Country：Japan  

  • 口腔健康の高齢社会への貢献　深圳歯科教育プログラム Invited

    武　洲

    深圳歯科教育プログラム  2018.6 

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    Event date： 2017.4 - 2018.6

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

    Venue：深圳   Country：Japan  

  • Oral health and healthy life expectancy Invited International conference

    Hiro Take

    The 1st International Symposium for Women Researchers on Advanced Science and Technology conjugated with Seminar for Young Researchers  2016.7 

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    Event date： 2016.7

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

    Venue：Kitakyushu   Country：Japan  

  • Oral health, Nutrition and healthy life expectancy Invited International conference

    Hiro Take

    9th CASPN  2015.5 

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    Event date： 2016.5

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

    Venue：Beijing   Country：China  

  • LPS from P. gingivalis enhances inflammatory responses of microglia during　exposure to amyloid ｂ

    Shuge Gui, Zhou Wu, Tomomi Sato, Takashi Kanematsu

    第97回日本薬理学会年会  2023.12 

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    Event date： 2024.12

    Language：English  

    Venue：神戸   Country：Japan  

    【Background】 Brain amyloid beta is accumulated from 20 years before Alzheimer's disease (AD) onset, and microglia is implicated in promoting AD pathogenesis. LPS from P. gingivalis (PgLPS), the periodontal bacteria, is detected in AD brain. 【Aim】 In this study, we test our hypothesis that PgLPS enhances microglia-mediated neuroinflammtion in amyloid beta exposure environment.【Methods & Results】 MG6 microglial cells were exposed to PgLPS (0.1 micro g/mL), amyloid beta (0.1micro M) or co-exposed to amyloid beta and PgLPS. Inflammatory mediators and NFkB signaling were examined. In comparison to control MG6 cells, mRNA expressions of TNF-α, IL-1beta and IL-6 were induced from 1 h after exposure to PgLPS but not amyloid beta. Interestingly, mRNA expressions of TNF-α, IL-1beta and IL-6 were significantly increased in amyloid beta and PgLPS co-exposed (AL) MG6 cells from 3 h in compassion to those in PgLPS-exposed cells. TNF-α production were significantly elevated in AL-exposed MG6 cells from 3 h in compassion to that in PgLPS-exposed ones. Furthermore, phosphorylation of IκB and nuclear translocation of p65 NF-κB were up-regulated in PgLPS-exposed MG6 cells but not that in amyloid beta-exposed cells. Phosphorylation of IκB and nuclear translocation of p65 NF-κB were significantly up-regulated in AL-exposed MG6 cells in compassion to that in PgLPS-exposed cells. 【Conclusion】 The observations strongly suggest that PgLPS enhances microglia-related neuroinflammtion in amyloid beta exposure environment. The present study provides a new mechanism of periodontitis involving in the early pathologies of AD.

  • P.gingivalis菌感染は髄膜細胞に誘導されるIL-1 beta を介してシナプス障害を引き起こす

    武　洲、桂　淑格、水谷 慎介、柏崎　晴彦

    第53回日本神経精神薬理学会  2023.9 

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    Event date： 2024.9

    Language：Japanese  

    Venue：東京   Country：Japan  

    背景と目的】歯周病は記憶低下と正相関することが報告されているが、その記憶低下への関与メカニズムには不明な点が多い。シナプス障害は記憶低下早期病態であり、我々は脳バリアの軟髄膜細胞（Leptomeningeal Cells, LC）が全身炎症に応答し、グリア細胞を活性化することを見出した。本研究では歯周病病原菌P. gingivalis (Pg)菌感染に伴うLCからシナプスに与える影響を明らかにする。【方法と結果】15ヶ月齢マウスを用いて、P.g菌感染後LCと大脳皮質ニューロン反応ならびに記憶力を調べた。また初代LCと初代皮質ニューロンを用いて、Pg菌感染したLCから産生分泌因子ならびにPg菌感染したLC培養上清(PgLCM)で処理した初代皮質ニューロンのシナプス関連因子を調べた。Pg菌に感染したマウスにおいて、軟髄膜における IL-1β発現が増加し、軟髄膜近接大脳皮質におけるシナプトフィジン (SYP) 発現が減少した。受動回避実験においてPg菌感染したマウスに躊躇行動が認められた。培養LCはPg菌を貪食しリソソームから細胞質にカテプシン B (CatB)漏出をもたらし、CatBは細胞質にてNLRP3インフラマソームを活性化させIL-1β産生分泌を誘導した。 一方、培養ニューロンにおいてPg LCM添加によりSYP などシナプス関連因子の発現が低下したが、それらの減少はIL-1 受容体アンタゴニストの前処理によって防げた。【結論】 結果からP. gingivalis菌感染により髄膜細胞にCatB/NLRP3インフラマソームに依存したIL-1β産生が誘導され、髄膜細胞からのIL-1βによってニューロンシナプス障害を引き起こすことが示唆された。歯周病病原菌による軟膜細胞を介したシナプス損傷は加齢やアルツハイマー病における認知機能低下を誘発し、加速させる可能性が考えられる。

  • 歯周病のアルツハイマー型認知症への関与メカニズム Invited

    武　洲

    長崎長崎県保険医協会  2024.2 

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    Event date： 2024.2

    Language：Japanese  

    Venue：オンライン   Country：Japan  

  • P.ジンジバリス菌は脳血管内皮細胞を介したamyloid 脳内流入を促進する

    武　洲、桂淑格、水谷慎介、柏崎晴彦

    第97回日本薬理学会年会  2023.12 

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    Event date： 2023.12

    Language：Japanese  

    Venue：神戸   Country：Japan  

  • P.gingivalis由来LPSが誘導する炎症に対するリコピンとキシリトールの抑制効果

    桂　淑格、高間　立、上野　功騎、五十野　貴大、行圓　元朗、武　洲、兼松　隆

    第65回歯科基礎医学会学術大会  2023.9 

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    Event date： 2023.9

    Language：Japanese  

    Venue：東京   Country：Japan  

    【目的】脳ストレスはニューロンにダメージを与えるが、可塑性に富む脳免疫細胞であるミクログリアの機能を制御できれば、脳内の恒常性を保つことができると言える。さて、免疫細胞の機能は、身近な食材成分によって調整することができる。本研究では、食材成分（リコピン、キシリトール）がミクログリア機能を制御できるかを検証し、食材による「脳ストレス緩和策」を提案する。「方法・結果」MG6細胞（mouse microglia cell line）を用いてP.gingivalis由来LPS （PgLPS）刺激後のTNFとIL-1の発現をリコピンやキシリトール添加によって変わるかを解析した。さらにMitoSOX Redを用いて、PgLPSによる酸化ストレス誘導に対するリコピン、キシリトールの作用効果を検討した。リコピン（～）やキシリトール（2%）の添加は、MG6細胞の生存に影響しなかった。MG6細胞をPgLPS（1 g/mL）で刺激するとTNF-とIL-1の発現は増加するが、その発現増加は2%キシリトール添加で有意に抑制できた。一方、10 Mリコピン添加では、TNF-発現は有意に抑制されたが、IL-1発現の抑制はみられなかった。興味深いことに、5 Mリコピンと1%キシリトールの併用添加によって、IL-1発現は有意に抑制された。酸化ストレス解析では、Control（PgLPS非刺激群）と比較して、PgLPS刺激群でMG6細胞のMitoSOX Redの蛍光強度は増加するが、5 Mリコピンと1％キシリトールとの併用添加により蛍光強度は有意に減少した。「結論」キシリトールとリコピンは、PgLPS処理によるミクログリアでのニューロン障害因子産生や酸化ストレス誘導を抑制することができる。また、キシリトールとリコピンのこの抑制効果には相加作用があることが明らかとなった。リコピンを多く含むトマトとキシリトールを多く含むイチゴなどを組み合わせて食事をすることにより、ストレスから脳を護ることができると考えられる。

  • Pathogenesis and intervention of dementia Invited International conference

    武　洲

    紹興文理学院医学部  2023.6 

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    Event date： 2023.6

    Language：Others   Presentation type：Oral presentation (general)  

    Venue：中国　紹興市   Country：China  

    Aging has become a global problem. As living standards improve, national life expectancy continues to increase. China's elderly population has exceeded 200 million, making it the only country in the world with an elderly population of over 100 million. The prevention and treatment of dementia, mainly Alzheimer's disease, has become a focus of geriatric medicine. Chronic peripheral inflammation can affect brain function through the sustained release of pro-inflammatory factors. Microglia, as innate immune cells in the brain, release pro-inflammatory factors to trigger brain inflammation and damage neurons after being activated by peripheral inflammatory signals. Our years of research have found that microglial activation-dependent brain inflammation induced by chronic peripheral inflammation can directly induce poor memory function. From this, we proposed the theory of "microglia aging", that is, microglia activation may be the key to accelerating brain aging.
    The harm of oral health disorders to systemic health has been widely studied. Research has confirmed that chronic periodontitis, as the most common chronic oral inflammation in middle-aged and elderly people, is involved in the occurrence and development of systemic diseases such as diabetes and osteoporosis. In recent years, studies have found that the severity of periodontal disease in the elderly is positively correlated with reduced cognitive function, and the main pathogenic bacteria of periodontitis, Porphyromonas gingivalis (P.g) endotoxin (LPS), has also been found in the brains of patients with Alzheimer's disease. was discovered in. Therefore, the impact of oral health on the brain has become a new hot topic in the fields of oral medicine, neuroscience, and geriatric medicine in Japan, Europe, and the United States.
    Nutrition is a decisive factor in maintaining body health, and the oral cavity is an important organ for nutritional intake. In recent years, we have proposed a new concept of "prolonging healthy life span through oral health". We believe that maintaining oral health can reduce systemic inflammation and inflammatory reactions in the brain through the intake of anti-inflammatory nutrients, and delay the decline of cognitive function. Japan is the most aging country in the world. In 2016, the population over 65 years old reached 29.1% of the total population, making it a super-aged society. We can gain a lot of experience by understanding and analyzing the current situation of Japan's aging society. This time, we will elaborate on the new concept of "prolonging healthy lifespan through oral health", explore the connection between oral health and brain health, and introduce Japan's oral health and nutrition programs to improve healthy lifespan. We hope that by deeply understanding the importance of "oral health to brain health", we can open up new ideas for delaying brain aging, extending healthy life expectancy, and creating a healthy aging society.

  • 歯周病菌による脳内炎症とアルツハイマー病 Invited

    武　洲

    第97回日本生理学会大会  2020.3 

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    Event date： 2020.3

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

    Venue：誌上開催   Country：Japan  

    超高齢社会に突入した我が国では認知症が急増している。認知症の7割を占めるアルツハイマー病（AD）は発症してから治療法が確立されておらず、莫大な医療費と深刻な社会負担になっている。欧米臨床研究では、ADと歯周病との正相関が多く報告され、AD患者剖検脳から歯周病菌のP.ジンジバリス（Pg菌）LPSも検出された。歯周病とADに歯周病の関与について関心を集め、その因果関連の解明研究が急速に進んでいる。ADの発症及び病態進行には脳内におけるアミロイド（A）の蓄積、タウの過剰なリン酸化に起因して、ニューロン死に至るが、ミクログリアに依存した脳内炎症がAの形成・蓄積するたびにウタンの過剰なリン酸化を引き起こし、ニューロン死を促進する。私たちは長年渡って全身炎症による脳機能への影響について解析しており、慢性全身炎症により年齢依存した脳内炎症が誘発され、その脳内炎症が年齢依存した学習・記憶障害を引き起こすことを見出した。歯周病を慢性炎症と捉え、Pg菌（Pg菌LPS）に対して脳内炎症の応答がADの発症と病態進行への関与とそのメカニズムについて検討を進めてきた。
    これまでの一連の研究により、Pg菌の全身感染（Pg菌LPS）に対して中年マウスにおいてミクログリアに依存した脳内炎症を起因し、ニューロン内にA蓄積ならびに学習・記憶障害というAD様病態を誘発することを発見し、リソソーム性タンパク質分解酵素のカテプシン（Cat）BはAD病態誘発の関連酵素と突き止めた。さらにCatSはPg菌染（Pg菌LPS）による全身炎症の増大関連酵素であることを明らかにした。本シンポジウムは私たちの歯周病菌による惹起された脳内炎症がアルツハイマー病への関与メカニズムにいて解説すると共に脳内炎症と全身炎症の制御による認知機能の改善につながる臨床研究も紹介する。
    加齢に連れて発症率が増加するADが発症してから根本的な治療は開発されていないため、その発症と病態進行を遅らせるには、口腔や全身炎症の早期介入は先制医療アプローチとして大きな意義があると考えられる。更に脳内炎症とその引き金である全身炎症の緩和にCatBとCatSの制御に期待したい。

  • An impaired intrinsic microglial clock system induces neuroinflammatory alterations in the early stage of amyloid precursor protein knock-in mouse brain

    Junjun Ni, Hiroshi Nakanishi and Zhou Wu

    第72回日本薬理学会西南部会  2019.11 

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    Event date： 2019.11

    Language：English   Presentation type：Oral presentation (general)  

    Venue：Naha   Country：Japan  

  • Mechanism of Cathepsins involving Alzheimer’s disease: Linking systemic inflammation & neuroinflammation Invited International conference

    武　洲

    北理工大学教育セミナー  2017.11 

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    Event date： 2018.6

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

    Country：Japan  

  • ミクログリアによる脳炎症を主軸とする歯周病のアルツハイマー病増悪メカニズムの解明

    武　洲

    第90回日本薬理学会年会・年会企画シンポジウム  2017.3 

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    Event date： 2018.6

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：長崎   Country：Japan  

  • 歯周病菌によるアルツハイマー様脳病態の発症と原因酵素としてのカテプシン群の役割

    武　洲

    第58回歯科基礎医学会学術大会・学術シンポジウム  2017.9 

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    Event date： 2018.6

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：塩尻   Country：Japan  

  • The Profound Impact of Oral health on Aging Societ Invited International conference

    Hiro Take

    吉林大学歯学部創立30周年　学術大会  2015.5 

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    Event date： 2016.5

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

    Venue：Chang chun   Country：China  

  • 歯周病とアルツハイマー病（AD）（1）： Porphyromonas gingivalis由来LPSによるマクロファージ活性化と脳髄膜を介した末梢炎症シグナルの脳内伝播とミクログリア活性化

    Yicong Liu, 武 洲, 中西 博

    第57回歯科基礎医学会  2015.9 

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    Event date： 2015.9

    Language：English   Presentation type：Oral presentation (general)  

    Venue：新潟   Country：Japan  

  • ATPならびにPorphyromonas gingivalis　（ＰＧ）局注注入により惹起されるミクログリア突起の集積とその日内変化に関する生体イメージング解析

    武 洲, 林 良憲, 中西 博, 髙山扶美子

    第57回歯科基礎医学会  2015.9 

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    Event date： 2015.9

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：新潟   Country：Japan  

  • 歯周病とアルツハイマー病（AD）（2）：Porphyromonas gingivalis由来LPSの慢性的末梢投与によって誘発されるAD様フェノタイプにおけるカテプシンBの役割

    武 洲, NI JUNJUN, 中西 博

    第57回歯科基礎医学会  2015.9 

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    Event date： 2015.9

    Language：English   Presentation type：Oral presentation (general)  

    Venue：新潟   Country：Japan  

  • Involvement of brain pericyte damage in neuropathological changes associated with lysosomal storage International conference

    Hiro Take, Ryo Okada, NI JUNJUN, Hiroshi Nakanishi

    International Conference on Neurology & Therapeutics  2015.7 

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    Event date： 2015.7

    Language：English  

    Venue：Rome   Country：Italy  

  • 歯周病によるアルツハイマー様病態の促進メカニズム

    武 洲, 中西 博

    第87回日本薬理年会  2015.3 

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    Event date： 2015.3

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

    Venue：名古屋   Country：Japan  

  • 歯周病菌による脳髄膜を介したミクログリアの活性化

    武 洲, 中西 博

    第56回歯科基礎医学会学術大会、  2014.9 

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    Event date： 2014.9

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

    Venue：福岡   Country：Japan  

  • The　possible link between periodontitis and Alzheimer’s Disease Invited International conference

    武 洲, Hiroshi Nakanishi

    中国薬理学会・老年医学会・認知機能障害と関連疾患シンポジウム  2014.8 

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    Event date： 2014.8

    Language：Others   Presentation type：Oral presentation (general)  

    Venue：Xining, Qinhai,   Country：China  

  • Porphyromonas gingivalis LPS induces microglial activation and A beta accumulation in the brain　DepartmentCathepsin B-dependent novel IL-1beta production pathway in microglia, Invited International conference

    Hiro Take

    Kudai Oral Bioscience 2014  2014.3 

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    Event date： 2014.2 - 2014.3

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

    Venue：福岡   Country：Japan  

  • クロモグラニンAによるミクログリアにおけるカテプシンB依存した新規IL-1beta 産生経路の解明

    武 洲, 中西 博

    第55回歯科基礎医学学術大会,  2013.9 

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    Event date： 2013.9

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：岡山   Country：Japan  

  • Cathepsin B-dependent　Novel IL-1β Production Pathway in Microglia Invited International conference

    Hiro Take, Hiroshi Nakanishi

    Kyudai Oral Bioscience 2013  2012.3 

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    Event date： 2012.3

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

    Venue：福岡   Country：Japan  

  • ミクログリアの産生するカテプシンBの炎症性慢性疼痛における役割

    武 洲, 中西 博, 林 良憲

    第85回日本薬理学会年会  2012.3 

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    Event date： 2012.3

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：京都   Country：Japan  

  • 末梢炎症によるミクログリア活性化と脳老化の促進

    武　洲、劉　霞、中西　博、

    第14回グリア研究会  2011.11 

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    Event date： 2011.11

    Venue：大阪   Country：Japan  

  • ホスファチジルセリンリポソームによる炎症性骨破壊抑制メカニズムの解析

    武　洲、馬　紅梅、久木田敏夫、中西　博

    第52回　歯科基礎医学会・学術大会・総会  2011.9 

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    Event date： 2011.9

    Language：Japanese  

    Venue：東京   Country：Japan  

  • 中年ルイスラットにおけるアジュバント関節炎に伴うミクログリア活性化と海馬長期増強の障害

    武　洲、劉　霞、中西　博

    第63回日本薬理学会西南部会  2010.11 

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    Event date： 2011.7

    Language：Japanese  

    Venue：鹿児島   Country：Japan  

  • Reverse of the rheumatoid arthritis-induced acceleration of brain aging in the middle age by minocycline. International conference

    Wu Z, Liu X, Nakanishi H.

    The 1st International Congress on Controversies in Longevity, Health and Aging.  2010.6 

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    Event date： 2011.6 - 2011.7

    Venue：バルセロナ   Country：Spain  

  • Microglial cathepsin B: A strategic target for neuroprotective agents. Invited International conference

    Wu Z, Nakanishi H.

    BIT’s Inaugural Symposium on Enzyme & Biocatalysis-2010  2011.7 

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    Event date： 2011.4 - 2011.7

    Presentation type：Symposium, workshop panel (public)  

    Venue：上海   Country：China  

  • 末梢炎症により誘発される髄膜を介したグリア反応の老化に伴う変容

    武　洲、　徳田　幸恵、張　馨文、中西　博

    第82回日本薬理学会年会  2009.3 

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    Event date： 2009.3

    Venue：横浜　パジフイコ横浜   Country：Japan  

  • Age-dependent differentiatial regulation of tight junction proteins in the leptomeninges by glial cells during systemic inflammation. International conference

    Wu Z, Nakanishi H.

    Neuroscience 2008  2008.11 

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    Event date： 2008.11

    Language：English   Presentation type：Oral presentation (general)  

    Country：United States  

    Age-dependent differentiatial regulation of tight junction proteins in the leptomeninges by glial cells during systemic inflammation.

  • 破骨前駆細胞の貪食機能に着目した新たな骨破壊抑制法

    武　洲、馬　紅梅、中西　博

    歯科基礎医学会  2008.9 

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    Event date： 2008.9

    Presentation type：Oral presentation (general)  

    Venue：東京   Country：Japan  

    Phosphatidylserine-containing liposomes inhibit the differentiation of osteoclasts and trabecular bone loss

  • Age-dependent differential modulation of the barrier function of the leptomeninges in the cerebral cortex by activated glial cells during the systemic inflammation International conference

    Zhou Wu, Yukie Tokuda, Xin-Wen Zhang, and Hiroshi Nakanishi

    XXVI CINP CONGRESS  2008.7 

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    Event date： 2008.7

    Language：English   Presentation type：Oral presentation (general)  

    Venue：Ｍunich   Country：Germany  

  • アジュバント関節炎ラットにおける骨棘の形成と知覚神経

    武　洲、永田　健吾、飯島　忠彦

    第５５回解剖学会九州支部会  1999.10 

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    Presentation type：Oral presentation (general)  

    Venue：熊本   Country：Japan  

  • アジュバント関節炎ラット距腿関節滑膜における神経成長因子及びレセプターの発現

    武　洲、永田　健吾、飯島　忠彦

    第４２回歯科基礎医学会  2000.9 

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    Presentation type：Oral presentation (general)  

    Venue：大阪   Country：Japan  

  • アジュバント関節炎ラット距腿関節滑膜における神経成長因子産生細胞について

    武　洲、永田　健吾、飯島　忠彦

    第一回西日本骨・関節関連疾患懇話会  2001.7 

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    Presentation type：Oral presentation (general)  

    Venue：福岡   Country：Japan  

  • ジュバント関節炎ラットにおける骨棘の形成と知覚神経

    武　洲、永田　健吾、飯島　忠彦

    2002.7 

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    Venue：福岡   Country：Japan  

  • アジュバント関節炎ラットにおける骨発壊機構：　CCケモカインMIP-αによる破骨細胞プロジェ二ターの骨破壊部への遊走と、破骨細胞様多核巨細胞塊におけるRANKLの発現

    藤　加寿子、久木田　敏夫、久木田　明子、武　洲、野見山　尚之、飯島忠彦

    第三回西日本骨・関節関連疾患懇話会  2003.7 

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    Presentation type：Oral presentation (general)  

    Venue：福岡   Country：Japan  

  • ットアジュバント関節炎に対する防已黄耆湯（TJ-20）の効果

    武　洲、飯島忠彦

    第１６回日本疼痛漢方研究会  2003.7 

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    Presentation type：Oral presentation (general)  

    Venue：東京   Country：Japan  

  • アジュバント関節炎に対する防已黄耆湯（TJ-20）の効果：滑膜における炎症性サイトカインおよび抗炎症性サイトカインの発現

    武　洲、飯島忠彦

    第１７回日本疼痛漢方研究会  2004.7 

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    Presentation type：Oral presentation (general)  

    Venue：東京   Country：Japan  

  • アジュバント関節炎ラット距腿関節滑膜中のヘルパーT細胞（Th1、Th2）の消長と坐骨神経

    武　洲、永田　健吾、久木田　敏夫、飯島　忠彦

    第四回西日本骨・関節関連疾患懇話会  2004.7 

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    Presentation type：Oral presentation (general)  

    Venue：福岡   Country：Japan  

  • 末梢炎症の際グリア細胞活性に軟膜細胞の関与

    武　洲、中西　博

    第１０回グリア研究会  2005.9 

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    Presentation type：Oral presentation (general)  

    Venue：大阪   Country：Japan  

  • 脳髄膜細胞の産生分泌する液性因子によるグリア細胞の活性化

    武　洲、中西　博

    第５８回日本薬理学会西南部会  2005.11 

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    Presentation type：Oral presentation (general)  

    Venue：長崎   Country：Japan  

  • 髄膜細胞から産生分泌されるＰＧＥ２を介したニューロン・グリア細胞におけるＴＧＦｂ１の発現

    武　洲、中西　博

    第５９回日本薬理学会西南部会  2006.11 

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    Presentation type：Oral presentation (general)  

    Venue：沖縄   Country：Japan  

  • 髄膜細胞によるＰＧＥ２を介したニューロン・グリア細胞におけるＴＧＦｂ１の発現制御

    武　洲、中西　博

    グリア研究会  2006.11 

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    Presentation type：Oral presentation (general)  

    Venue：東京   Country：Japan  

  • 病者行動の加齢に伴う増悪におけるグリア炎症反応の関与

    新道　まゆみ、　武　洲、　馬　紅梅、　中西　博

    第二回「口腔健康科学」シンポジウム  2007.2 

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    Presentation type：Symposium, workshop panel (public)  

    Venue：Fukuoka   Country：Japan  

  • Intra-arterial injected microglia engraft in the brain to rescue neuronal damage International conference

    Y.Hayashi, J.Yamada, Z.Wu, M.Sawada and H.Nakanishi

    The 2nd symposium on " Dental and Craniofacial Morphogenesis and Tissue Regeneration"  2007.3 

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    Presentation type：Oral presentation (general)  

    Venue：Fukuoka   Country：Japan  

  • Gatekeeper of chronic inflammation: Cathepsin B-dependent Novel IL-1beta Production Pathway Invited International conference

    Hiro Take

    School of Stomalogy, Jilin University, Changchun, China,  2013.3 

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

    Venue：School of Stomalogy, Jilin University, Changchun, China,   Country：Japan  

  • Gatekeeper of chronic inflammation: Cathepsin B-dependent Novel IL-1beta Production Pathway Invited International conference

    Hiro Take

    School of Stomalogy, Jilin University, Changchun, China,  2013.3 

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

    Venue：School of Stomalogy, Jilin University, Changchun, China,   Country：Japan  

  • Potential roles of chromogranin A in cathepsin B-dependent　IL-1bata production by microglia in Alzheimer’s disease,

    Hiro Take, Hiroshi Nakanishi

    第86回日本薬理学会年会  2013.3 

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    Language：English   Presentation type：Oral presentation (general)  

    Venue：福岡   Country：Japan  

  • 口腔から考える認知症予防 Invited

    武 洲

    日本抗加齢医学会総会プログラム・抄録集  2023.6  (一社)日本抗加齢医学会

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

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MISC

  • mtDNA Maintenance and Alterations in the Pathogenesis of Neurodegenerative Diseases Reviewed

    Dehao Shang, Minghao Huang, Biyao Wang, Xu Yan, ＠Zhou Wu, Xinwen Zhang

    Current Neuropharmacology   2023.4

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    Language：English   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

    Considerable evidence indicates that the semiautonomous organelles mitochondria play key roles in the progression of many neurodegenerative disorders. Mitochondrial DNA (mtDNA) encodes components of the OXPHOS complex but mutated mtDNA accumulates in cells with aging, which mirrors the increased prevalence of neurodegenerative diseases. This accumulation stems not only from the misreplication of mtDNA and the highly oxidative environment but also from defective mitophagy after fission. In this review, we focus on several pivotal mitochondrial proteins related to mtDNA maintenance (such as ATAD3A and TFAM), mtDNA alterations including mtDNA mutations, mtDNA elimination, and mtDNA release-activated inflammation to understand the crucial role played by mtDNA in the pathogenesis of neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and Huntington's disease. Our work outlines novel therapeutic strategies for targeting mtDNA.

    DOI： 10.2174/1570159X20666220810114644

  • Cathepsin B Gene Knockout Improves Behavioral Deficits and Reduces Pathology in Models of Neurological Disorders Reviewed

    Gregory Hook, Thomas Reinheckel, Junjun Ni, ＠Zhou Wu, Mark Kindy, Christoph Peters, and Vivian Hook

    2022.7

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    Language：English   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

    Cathepsin B (CTSB) is a powerful lysosomal protease. This review evaluated CTSB gene knockout (KO) outcomes for amelioration of brain dysfunctions in neurologic diseases and aging animal models. Deletion of the CTSB gene resulted in significant improvements in behavioral deficits, neuropathology, and/or biomarkers in traumatic brain injury, ischemia, inflammatory pain, opiate tolerance, epilepsy, aging, transgenic Alzheimer’s disease (AD), and periodontitis AD models as shown in 12 studies. One study found beneficial effects for double CTSB and cathepsin S KO mice in a multiple sclerosis model. Transgenic AD models using amyloid precursor protein (APP) mimicking common sporadic AD in three studies showed that CTSB KO improved memory, neuropathology, and biomarkers; two studies used APP representing rare familial AD and found no CTSB KO effect, and two studies used highly engineered APP constructs and reported slight increases in a biomarker. In clinical studies, all reports found that CTSB enzyme was upregulated in diverse neurologic disorders, including AD in which elevated CTSB was positively correlated with cognitive dysfunction. In a wide range of neurologic animal models, CTSB was also upregulated and not downregulated. Further, human genetic mutation data provided precedence for CTSB upregulation causing disease. Thus, the consilience of data is that CTSB gene KO results in improved brain dysfunction and reduced pathology through blockade of CTSB enzyme upregulation that causes human neurologic disease phenotypes. The overall findings provide strong support for CTSB as a rational drug target and for CTSB inhibitors as therapeutic candidates for a wide range of neurologic disorders.

    DOI： 10.1124/pharmrev.121.000527

  • The Dual Nature of Microglia in Alzheimer's Disease: A Microglia-Neuron Crosstalk Perspective. Reviewed

    Zhen Xie, Jie Meng, @Zhou Wu, Hiroshi Nakanishi, Yoshinori Hayashi, Wei Kong, Fei Lan, Narengaowa, Qinghu Yang, Hong Qing, Junjun Ni

    Neuroscientist   2022.3

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    Language：English   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

    DOI： doi: 10.1177/10738584211070273

  • 歯周病がアルツハイマー病の原因に？！歯科から始めるザ・認知症予防 Reviewed

    武　洲

    nico QUINTESSENCE PUBLISHING   2021.7

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    Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

  • 認知症に備える Reviewed

    武　洲

    Re　一般財団法人　建築保全センター   2021.5

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    Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

    認知症の7割を占めるアルツハイマー型認知症（Alzheimer's disease,AD）の9割は加齢に連れて発症し、わが国の認知症増加の一因と考えられる。脳内免疫細胞のミクログリア異常に惹起される脳内炎症がアミロイドβ（A）蓄積を促す。一方、関節リウマチなど疾患に増大される全身炎症がミクログリア異常を起こし、ADの発症や病態進行を加速することも分かっている。中高年の8割に発症する歯周病は全身に炎症を起こし、近年ADへの関与が注目されている。
    本稿では歯周病のADへの関与機序を解説し、認知症の備えに口を衛（まもる）から脳を守る「口健力」創出という理念を提案する。

  • Inflammation Spreading: Negative Spiral Linking Systemic Inflammatory Disorders and Alzheimer's Disease Reviewed

    Junjun Ni, ＠Zhou Wu.

    Front Cell Neurosci.   2021.5

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    Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

    As a physiological response to injury in the internal body organs, inflammation is responsible for removing dangerous stimuli and initiating healing. However, persistent and exaggerative chronic inflammation causes undesirable negative effects in the organs. Inflammation occurring in the brain and spinal cord is known as neuroinflammation, with microglia acting as the central cellular player. There is increasing evidence suggesting that chronic neuroinflammation is the most relevant pathological feature of Alzheimer's disease (AD), regulating other pathological features, such as the accumulation of amyloid-β (Aβ) and hyperphosphorylation of Tau. Systemic inflammatory signals caused by systemic disorders are known to strongly influence neuroinflammation as a consequence of microglial activation, inflammatory mediator production, and the recruitment of peripheral immune cells to the brain, resulting in neuronal dysfunction. However, the neuroinflammation-accelerated neuronal dysfunction in AD also influences the functions of peripheral organs. In the present review, we highlight the link between systemic inflammatory disorders and AD, with inflammation serving as the common explosion. We discuss the molecular mechanisms that govern the crosstalk between systemic inflammation and neuroinflammation. In our view, inflammation spreading indicates a negative spiral between systemic diseases and AD. Therefore, "dampening inflammation" through the inhibition of cathepsin (Cat)B or CatS may be a novel therapeutic approach for delaying the onset of and enacting early intervention for AD.

    DOI： doi: 10.3389/fncel.2021.638686. eCollection 2021

  • Glia-driven neuroinflammation and systemic inflammation in Alzheimer's disease. Reviewed

    Hashioka S, Wu Z, Klegeris A.

    Curr Neuropharmacol .   2020.11

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    Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

    The neuroinflammatory hypothesis of Alzheimer's disease (AD) was proposed more than 30 years ago. The involvement of the two main types of glial cells, microglia and astrocytes, in neuroinflammation was suggested early on. In this review we highlight that the exact contributions of reactive glia to AD pathogenesis remain difficult to define likely due to the heterogeneity of glia populations and alterations in their activation states through the stages of AD progression. In the case of microglia, it is becoming apparent that both beneficially and adversely activated cell populations can be identified at various stages of AD, which could be selectively targeted to either limit their damaging actions or enhance beneficial functions. In the case of astrocytes, less information is available about potential subpopulations of reactive cells; it also remains elusive whether astrocytes contribute to the neuropathology of AD by mainly gaining neurotoxic functions or losing their ability to support neurons due to astrocyte damage. We identify L-type calcium channel blocker, nimodipine, as a candidate drug for AD, which potentially targets both astrocytes and microglia. It has already shown consistent beneficial effects in basic experimental and clinical studies. We also highlight the recent evidence linking peripheral inflammation and neuroinflammation. Several chronic systemic inflammatory diseases, such as obesity, type 2 diabetes mellitus, and periodontitis, can cause immune priming or adverse activation of glia thus exacerbating neuroinflammation and increasing risk or facilitating progression of AD. Therefore, reducing peripheral inflammation is a potentially effective strategy for lowering AD prevalence.

    DOI： doi: 10.2174/1570159X18666201111104509.

  • 歯周病とアルツハイマー病型認知症 Reviewed

    武　洲

    保健の科学   2020.6

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    Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

  • 歯周病感染がマクロファージにおけるアミロイドβの産生を引き起こす可能性（トピックス） Reviewed

    武　洲

    バイオサイエンスとインダストリー（B&I)   2020.6

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    Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

  • Involvement of Cathepsins in Innate and Adaptive Immune Responses in Periodontitis Reviewed

    Xu Yan;＠Zhou Wu;Biyao Wang;Tianhao Yu; Yue Hu; Sijian Wang;Chunfu Deng; Baohong Zhao; Hiroshi Nakanishi and Xinwen Zhan

    Evidence-Based Complementary and Alternative Medicine   2020.3

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    Language：English   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

    Periodontitis is an infectious disease whereby the chronic inflammatory process of the periodontium stimulated by bacterial products induces specific host cell responses. The activation of the host cell immune system upregulates the production of　inflammatorymediators,comprisingcytokinesandproteolyticenzymes,whichcontributetoinflammationandbonedestruction.Ithasbeenwellknownthatperiodontitisisrelatedtosystemicinflammationwhichlinkstonumeroussystemicdiseases,includingdiabetesandarteriosclerosis.Furthermore,periodontitishasbeenreportedinassociationwithneurodegenerativediseasessuchasAlzheimer’sdisease(AD)inthebrain.Regardingimmuneresponsesandinflammation,cathepsinB(CatB)playspivotalrolefortheinductionofIL-1β,cathepsinK-(CatK-)dependentactivetoll-likereceptor9(TLR9)signaling,andcathepsinS(CatS)which involves in regulating both TLR signaling and maturation of the MHC class II complex. Notably, both the production and proteolytic activities of cathepsins are upregulated in chronic inflammatory diseases, including periodontitis. In the present review, we focus on the roles of cathepsins in the innate and adaptive immune responses within periodontitis. We believe that　understandingtherolesofcathepsinsintheimmuneresponsesinperiodontitiswouldhelptoelucidatethetherapeuticstrategies of periodontitis, thus benefit for reduction of systemic diseases as well as neurodegenerative diseases in the global aging society.

    DOI： doi.org/10.1155/2020/4517587

  • 歯周病のアルツハイマー病における関与メカニズム

    武　洲、中西　博

    細胞   2018.6

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    Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

  • 古くて新しいアルツハイマー病の脳炎症仮説と感染症仮説：鍵を握るミクログリアの老化と慢性的脳炎症

    武　洲、中西　博

    日本薬理誌   2017.6

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    Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

  • 歯周病のアルツハイマー病における関与メカニズム：慢性全身性炎症からミクログリア活性化脳炎症へ

    武　洲、中西　博

    BIO Clinica   2017.6

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    Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

  • Nutrients, Microglia Aging, and Brain Aging

    Wu Z, Yu J, Zhu A, Nakanishi H

    Oxid Med Cell Longev   2016.6

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    Language：English   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

  • 歯周病菌が認知症に与える影響 Reviewed

    武　洲

    デンタルダイアモンド誌   2021.4

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    Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

  • Microglial cathepsin B and Porphyromonas gingivalis gingipains as potential therapeutic targets for sporadic Alzheimer's disease. Reviewed

    Hiroshi Nakanishi , Saori Nonaka , ＠Zhou Wu.

    CNS Neurol Disord Drug Targets.   2020.7

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    Language：English   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

    DOI： 10.2174/1871527319666200708125130

  • 歯周病とアルツハイマー型認知症 Reviewed

    武　洲

    保健の科学   2020.7

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    Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

  • Lessons from Microglia Aging for the Link between Inflammatory Bone Disorders and Alzheimer's Disease.

    Wu Z, Hiroshi Nakanishi

    J Immunol Res   2015.5

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    Language：English   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

  • Connection between periodontitis and Alzheimer's disease: possible roles of microglia and leptomeningeal cells

    Wu Z, Hiroshi Nakanishi

    J Pharmacol Sci.   2014.8

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    Language：English   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

  • Preventing and Reversing “Microglia-Aging” by Nature Elements for Slow Brain- Aging

    Wu Z, Zhu A, Wu S, Hiroshi Nakanishi

    J Neurological Disorders. 2013 2：1：1000143   2013.12

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    Language：English   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

  • The role of microglial mtDNA damage in age-dependent prolonged LPS-induced sickness behavior.

    Hiroshi Nakanishi, Yoshinori Hayashi, Wu Z

    Neuron Glia Biol. 216:133-42   2011.2

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    Language：English   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

  • Phosphatidylserine-containing liposomes: potential pharmacological interventions against inflammatory and immune diseases through the production of prostaglandin E(2) after uptake by myeloid derived phagocytes.

    Wu Z, Nakanishi H.

    Arch Immunol Ther Exp   2011.1

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    Language：English   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

  • Microglia-aging: Roles of microglial lysosome- and mitochondria-deroved reactive oxygen species in brain aging. Behav. Brain Res.

    Nakanishi H. and Wu Z.

    Behav. Brain Res. Behav Brain Res.   2009.7

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    Language：English   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

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Professional Memberships

  • 歯科基礎医学会

  • 日本薬理学会

  • Socitity of Neuroscience

  • Asian College of Neuropsychopharmacology

  • 日本神経精神薬理学会

Academic Activities

  • 講演

    長崎県保険医協会講演会  （ Japan ） 2024.2

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    Type：Competition, symposium, etc. 

    Number of participants：80

  • シンポジウム講演

    全国保険医団体連合会シンポジウム  （ Japan ） 2023.10 - 2024.4

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    Type：Competition, symposium, etc. 

    Number of participants：500

  • シンポジウム　講演

    第23回日本抗加齢医学会総会  （ Japan ） 2023.6

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    Type：Competition, symposium, etc. 

    Number of participants：900

  • 健康かながわ

    2023.3 - 2023.4

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    Type：Academic society, research group, etc. 

  • Screening of academic papers

    Role(s)： Peer review

    2023

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    Type：Peer review 

    Number of peer-reviewed articles in foreign language journals：6

  • 座長 International contribution

    Kyudai Oral Bioscience & OBT Research Center 6th Joint International Symposium 2022  （ Japan ） 2022.10 - 2021.10

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    Type：Competition, symposium, etc. 

    Number of participants：60

  • シンポジウム　講演

    第11回日本認知症予防学会  （ Japan ） 2022.9 - 2021.9

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    Type：Competition, symposium, etc. 

    Number of participants：1,000

  • 特別講演 International contribution

    国際医科学研究会 第20回フォーラム  （ Japan ） 2022.6

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    Type：Competition, symposium, etc. 

    Number of participants：100

  • 特別講演

    兵庫県保険医協会神戸支部講演会  （ Japan ） 2022.4

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    Type：Competition, symposium, etc. 

    Number of participants：90

  • 特別講演

    愛知学院歯学部同窓会愛知県支部学術講演会  （ Japan ） 2022.2 - 2022.6

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    Type：Competition, symposium, etc. 

    Number of participants：80

  • 記念シンポジウム講演

    第 30 回 日本病態生理学会大会  （ Japan ） 2022.1

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    Type：Competition, symposium, etc. 

    Number of participants：120

  • Screening of academic papers

    Role(s)： Peer review

    2022

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    Type：Peer review 

    Number of peer-reviewed articles in foreign language journals：6

  • SJWS奨励-記念受賞講演

    第26回日本女性科学者の会奨励賞贈呈式  （ Japan ） 2021.9

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    Type：Competition, symposium, etc. 

    Number of participants：120

  • 特別講演

    福岡県歯科保険医協会 市民公開講演会  （ Japan ） 2021.9

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    Type：Competition, symposium, etc. 

    Number of participants：150

  • 特別講演 International contribution

    Q-AOS Brown Bag Seminar  （ Japan ） 2021.8

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    Type：Competition, symposium, etc. 

    Number of participants：120

  • シンポジウム　講演

    認知症と口腔機能研究会・JRSDOF第2回学術集会  （ Japan ） 2021.8

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    Type：Competition, symposium, etc. 

    Number of participants：60

  • 特別講演 International contribution

    SNU – KYUSHU JOINT SYMPOSIUM  （ Japan ） 2021.6

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    Type：Competition, symposium, etc. 

    Number of participants：70

  • シンポジウム　講演

    第97回日本生理学会大会  （ Japan ） 2021.4

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    Type：Competition, symposium, etc. 

  • 特別講演　座長 International contribution

    Kyudai Oral Bioscience & OBT Research Center Joint International Symposium 2021  （ Fukuoka Japan ） 2021.2

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    Type：Competition, symposium, etc. 

    Number of participants：70

  • 特別講演　座長 International contribution

    Kyudai Oral Bioscience & OBT Research Center Joint International Symposium 2021  （ Fukuoka Japan ） 2021.2

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    Type：Competition, symposium, etc. 

    Number of participants：80

  • 特別講演

    福岡県歯科保険医協会 北九州支部世話人会主催 ウェブ講演会  （ Japan ） 2021.1

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    Type：Competition, symposium, etc. 

    Number of participants：40

  • Screening of academic papers

    Role(s)： Peer review

    2021

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    Type：Peer review 

    Number of peer-reviewed articles in foreign language journals：6

  • シンポジウム　講演

    第116回日本精神神経学会学術総会  （ Japan ） 2020.9

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    Type：Competition, symposium, etc. 

    Number of participants：500

  • 特別講演

    九州口腔衛生学会総会シンポジウム  （ Japan ） 2020.9

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    Type：Competition, symposium, etc. 

    Number of participants：80

  • 特別講演　座長 International contribution

    Kyudai Oral Bioscience & OBT Research Center Joint International Symposium 2020  （ Fukuoka Japan ） 2020.2

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    Type：Competition, symposium, etc. 

  • Screening of academic papers

    Role(s)： Peer review

    2020

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    Type：Peer review 

    Number of peer-reviewed articles in foreign language journals：5

  • シンポジウム座長 International contribution

    6th Congress of AsCNP  （ Fukuoka Japan ） 2019.10

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    Type：Competition, symposium, etc. 

    Number of participants：2,200

  • Committees & Organizers, keynote speaker International contribution

    Neurology, Neuroscience and Neuromuscular disorders  （ Tokyo Japan ） 2019.6

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    Type：Competition, symposium, etc. 

    Number of participants：60

  • Committees & Organizers, session chair International contribution

    KOB2019  （ Fukuoka Japan ） 2019.2 - 2019.3

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    Type：Competition, symposium, etc. 

    Number of participants：80

  • Screening of academic papers

    Role(s)： Peer review

    2019

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    Type：Peer review 

    Number of peer-reviewed articles in foreign language journals：5

  • speaker, Committees & Organizers International contribution

    KOB2018  （ Fukuoka Japan ） 2018.2 - 2019.6

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    Type：Competition, symposium, etc. 

    Number of participants：100

  • 座長

    第90回日本薬理学会年会  （ Japan ） 2017.3

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    Type：Competition, symposium, etc. 

  • chair person International contribution

    KOB 2016  （ Fukuoka Japan ） 2016.2

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    Type：Competition, symposium, etc. 

    Number of participants：120

  • 座長（Chairmanship） International contribution

    the 6th international joint symposium on“dental and craniofacial morphogenesis　and tissue regeneration”and“oral health science”  （ Fukuoka Recent Hotel,Fukuoka Japan ） 2011.3

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    Type：Competition, symposium, etc. 

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Research Projects

  • 京セラ共同研究

    2023 - 2026

    京セラ

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    Authorship：Coinvestigator(s)  Grant type：On-campus funds, funds, etc.

  • ジンジバリス菌による脳バリア微環境破綻を介したアルツハイマー病誘発機序の解明

    2022.4 - 2025.3

    九州大学（日本） 

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    Authorship：Principal investigator 

    Clinical research has shown that there is a positive correlation between periodontal disease and the progression of Alzheimer's disease (AD), and the components of periodontal pathogen P. gingivalis have been detected in autopsy brains of patients with AD. It has been proposed that periodontal disease is an exacerbating factor in AD, but its involvement in the early pathogenesis of AD is still unclear. We have consistently analyzed the effects of systemic inflammation, including periodontal disease, on brain function for many years. We have shown that P. gingivalis/LPS induces AD-like brain pathology and systemic pathology that promotes AD-like brain pathology in normal middle-aged mice. It has been discovered that amyloid (A) is imported into the brain via brain barrier cells, which are the interface between the circulating blood and the brain. Synaptic disorders are an extremely early pathological condition before the onset of AD. In this project, we investigated the effects of P. gingivalis on disruption of brain barrier microenvironment homeostasis, synaptic disorders as well as learning and memory functions. We aim to verify the involvement of periodontal disease in early AD pathology and elucidate its molecular mechanism.

  • Elucidating new mechanism of brain barrier-synaptic disruptions caused by P. gingivitis

    Grant number：22K09927  2022 - 2025

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

    武 洲

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    Authorship：Principal investigator  Grant type：Scientific research funding

    臨床研究により、歯周病がアルツハイマー病（AD）の増悪因子と示唆されているが、その増悪機序には不明な点が多い。シナプス障害はADの超早期病態であり、脳内に蓄積されるアミロイドｂ（Ab） がその障害を惹起する。一方、申請者は歯周病病原菌P.gingivalis菌が中年マウスの脳バリアにAb蓄積と記憶障害が誘発されることを発見したが、シナプスに与える影響が検証されていない。そこで本研究において、P.gingivalis菌による脳バリア構造と機能破綻の実証、脳バリアにおけるAbクリアランス機構崩壊、 脳バリア破綻によるシナプス障害について検討を行い、歯周病のAD発端になる新たな分子機序を解明する。

    CiNii Research

  • ニューロンの保護作用の研究開発

    2021

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    Grant type：Donation

  • ニューロンの保護作用の研究開発

    2020

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    Grant type：Donation

  • 株式会社バイオコクーン研究所

    2018.4 - 2020.3

    Joint research

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    Authorship：Principal investigator  Grant type：Other funds from industry-academia collaboration

  • ニューロンの保護作用の研究開発

    2018

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    Grant type：Donation

  • 口腔健康と認知機能の相関に関するチベット族中高年者を対象とした日中合同疫学調査

    Grant number：16H05848  2016 - 2018

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

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    Authorship：Principal investigator  Grant type：Scientific research funding

  • ミクログリアによる脳炎症を主軸とする歯周病のアルツハイマー病増悪メカニズムの解明

    Grant number：16K11478  2016 - 2018

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

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    Authorship：Principal investigator  Grant type：Scientific research funding

  • ミクログリア極性分子スイッチとしてのプロテアーゼ反応に着目した疼痛炎症病態の制御

    Grant number：15H05015  2015 - 2018

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

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    Authorship：Coinvestigator(s)  Grant type：Scientific research funding

  • 歯周パラ・インフラメーションから脳をまもる髄膜-グリア防御システム破綻の解明

    Grant number：24592802  2012 - 2015

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

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    Authorship：Principal investigator  Grant type：Scientific research funding

  • 歯周病の脳炎症誘導メカニズムならびにエイジングによる変容の解明

    2011 - 2012

    教育研究プログラム・研究拠点形成プロジェクト（P&P）

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    Authorship：Principal investigator  Grant type：On-campus funds, funds, etc.

  • 歯周病の脳炎症誘導メカニズムならびにエイジングによる変容の解明

    2011 - 2012

    教育研究プログラム・研究拠点形成プロジェクト（P&P）

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    Authorship：Principal investigator  Grant type：On-campus funds, funds, etc.

  • 末梢炎症時の髄膜傷害因子としてのIL-1βとその産生におけるカテプシンBの役割

    Grant number：20592174  2008 - 2010

    Grants-in-Aid for Scientific Research  Grant-in-Aid for General Research (C)

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    Authorship：Principal investigator  Grant type：Scientific research funding

  • 歯周病による脳炎症誘発および加齢に伴う増悪における「髄膜ーグリア連関」破錠の関与

    Grant number：19592171  2007 - 2008

    Grants-in-Aid for Scientific Research  Grant-in-Aid for General Research (C)

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    Authorship：Coinvestigator(s)  Grant type：Scientific research funding

  • 髄膜ーグリア細胞連関による三叉神経痛制御

    Grant number：18613010  2006 - 2007

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

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    Authorship：Principal investigator  Grant type：Scientific research funding

  • カテプシンD欠損による老化促進機序の解明と酵素補充による老化に関する研究

    Grant number：17390495  2005 - 2007

    Grants-in-Aid for Scientific Research  Grant-in-Aid for General Research (B)

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    Authorship：Coinvestigator(s)  Grant type：Scientific research funding

  • ミクログリアによるグルタミン酸を介した神経伝達の動的制御

    Grant number：15082204  2002 - 2007

    Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research on Priority Areas

    　 More details

    Authorship：Coinvestigator(s)  Grant type：Scientific research funding

▼display all

Educational Activities

  • Enforce the lectures for undergraduate and graduate students school as a faculty member, conducte research guidance for undergraduates and graduate studentsand write the research papers as PI (principle investigator).

Class subject

  • リサーチエクスポージャー

    2023.4 - 2023.9   First semester

  • 歯科薬理学

    2022.4 - 2023.3   Full year

  • アーリーエクスポージャー　　リサーチエクスポージャー

    2022.4 - 2023.3   Full year

  • アカデミック・フロンティアI、II

    2022.4 - 2022.9   First semester

  • 歯科薬理学

    2021.4 - 2022.3   Full year

  • 歯科薬理学

    2020.4 - 2021.3   Full year

  • 歯科薬理学

    2019.4 - 2020.3   Full year

  • 歯科薬理学

    2018.4 - 2019.3   Full year

  • 歯科薬理

    2017.4 - 2018.3   Full year

  • 歯科薬理

    2016.4 - 2016.9   First semester

  • 歯科薬理

    2015.4 - 2015.9   First semester

  • 歯科薬理学

    2014.4 - 2014.9   First semester

  • 歯科薬理学

    2013.4 - 2013.9   First semester

  • 歯科薬理学

    2012.4 - 2012.9   First semester

  • 歯科薬理学

    2011.10 - 2012.3   Second semester

  • 歯科薬理学

    2010.4 - 2010.9   First semester

  • 歯科薬理学

    2009.10 - 2010.3   Second semester

  • 歯科薬理学

    2009.4 - 2009.9   First semester

▼display all

FD Participation

  • 2024.9   Role：Participation   Title：馬出地区4部局合同男女共同参画FD/ 病院きらめきプロジェクト講演会

    Organizer：[Undergraduate school/graduate school/graduate faculty]

Visiting, concurrent, or part-time lecturers at other universities, institutions, etc.

  • 2021  日本医科大学  Classification:Part-time lecturer  Domestic/International Classification:Japan 

    Semester, Day Time or Duration：大学院特別講義

  • 2019  日本大学松戸歯学部  Classification:Part-time lecturer  Domestic/International Classification:Japan 

  • 2019  放送大学  Classification:Part-time lecturer  Domestic/International Classification:Japan 

Participation in international educational events, etc.

  • 2022.11

    中国老年疾患研究センター　青海省医師会老年医学科分会

    第一回高原地域老年脳健康促進研究会

    　 More details

    Venue：中国　西寧

    Number of participants：300

  • 2022.10

    九州大学歯学研究院

    Kyudai Oral Bioscience & OBT Research Center 6th Joint International Symposium 2022

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    Venue：日本福岡

    Number of participants：60

  • 2022.6

    国際医科学研究会

    第20回国際医科学研究会フォーラム

    　 More details

    Venue：日本　東京

    Number of participants：80

  • 2021.6

    九州大学・ソウル大学

    The 2nd SNU-KYUSHU JOINT ONLINE SYMPOSIUM　Lecture

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    Venue：日本（韓国）・福岡（ソウル）

    Number of participants：100

  • 2019.9

    吉林大学　（九州大学協定校）

    吉林大学白求恩医学部創立80周年記念式典　特別講演

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    Venue：中国吉林省長春市

    Number of participants：2,000

  • 2018.10

    Beijing Institute of Technology, School of Life Science

    Beijing Institute of Technology, special lecture

    　 More details

    Venue：China, Beijing

    Number of participants：100

  • 2017.11

    北理工大学

    招待講演

    　 More details

    Venue：中国・北京

    Number of participants：60

  • 2017.4

    深圳職業学院

    深圳歯科教育プログラム

    　 More details

    Venue：中国・深圳

    Number of participants：120

  • 2017.2

    University of Southampton

    招待講演

    　 More details

    Venue：イギリス・Southampton

    Number of participants：60

  • 2015.8

    青海省政府

    中国西部老年医学教育プロジェクト　招待講演

    　 More details

    Venue：中国　青海省西寧市

    Number of participants：200

  • 2015.6

    深圳龍崗中央病院

    中国国家級再教育プログラム　招待講演

    　 More details

    Venue：深圳　中国

    Number of participants：100

  • 2013.3

    吉林大学　歯学部

    大学特別講演会　講演者

    　 More details

    Venue：中国　長春

    Number of participants：100

  • 2012.8

    青海省政府・青海省人民病院

    青海チベット高原老年医学・脳神経医学研究者育成プロジェクト　招待講演

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    Venue：中国　西寧市

    Number of participants：300

  • 2012.3

    吉林大学　歯学部

    大学特別講演会　　講演者

    　 More details

    Venue：中国　長春

    Number of participants：100

▼display all

Other educational activity and Special note

  • 2023  Special Affairs  指導する大学院生桂淑格さんは大塚奨学金奨学生に採択された。

    　詳細を見る

    指導する大学院生桂淑格さんは大塚奨学金奨学生に採択された。

  • 2021  Special Affairs  リサーチエクスポージャー講義で指導した学部生（4人）の「口から引き出す免疫機能～歯科医学生からの提案～」という課題が、福岡県歯科保健医協会主催した市民公開講演会に出演し、社会に連携する歯学教育として高く評価されている。

    　詳細を見る

    リサーチエクスポージャー講義で指導した学部生（4人）の「口から引き出す免疫機能～歯科医学生からの提案～」という課題が、福岡県歯科保健医協会主催した市民公開講演会に出演し、社会に連携する歯学教育として高く評価されている。

  • 2020  Special Affairs  指導した大学院生の2名が（Zeng　Fan、Gu　Yebo) 2021年度、藤野賞（歯学府）ならびに学術研究活動表彰（九州大学）を受賞しした。

    　詳細を見る

    指導した大学院生の2名が（Zeng　Fan、Gu　Yebo) 2021年度、藤野賞（歯学府）ならびに学術研究活動表彰（九州大学）を受賞しした。

  • 2018  Special Affairs  指導した学部生（4人）の「健康日本を担う将来世代の教育絵本づくり〜予防医療を広める歯学生の積極的実践」という課題が、九州大学アイデア・バトル2018に採択され、絵本の原案として作成した紙芝居は、保育園やワークショップコレクションin福岡2019の九州大学特別講義などに出演し、社会に連携する歯学教育として高く評価されている。

    　詳細を見る

    指導した学部生（4人）の「健康日本を担う将来世代の教育絵本づくり〜予防医療を広める歯学生の積極的実践」という課題が、九州大学アイデア・バトル2018に採択され、絵本の原案として作成した紙芝居は、保育園やワークショップコレクションin福岡2019の九州大学特別講義などに出演し、社会に連携する歯学教育として高く評価されている。

  • 2018  Special Affairs  ワークショップコレクション in 福岡 2019　九州大学特別授業　（歯学部学部生　4人参加）

    　詳細を見る

    ワークショップコレクション in 福岡 2019　九州大学特別授業　（歯学部学部生　4人参加）

Outline of Social Contribution and International Cooperation activities

  • As a member of the Japan BPW (Business & Professional Woman) Federation Fukuoka Club (Niji no Kai), I strive to improve the social status and vocational standards of working women and educate female students through various activities. I had served as an officer of the Niji no Kai from 2019 to 2021(planning and international affairs), and I has been a member of the International and Development Committee of the International Women's Year Liaison Committee since 2021. We also hold seminars for citizens all over the country through the Private Grant Foundation. He is in charge of managing and giving lectures on international symposiums held at the Institute of Dentistry, giving lectures overseas, and conducting joint research with overseas.

Social Activities

  • 歯周病とアルツハイマー型認知症の結びつき

    東京都立心身障害者口腔保健センター  オンライン  2023.10

    　More details

    Audience：General,　Scientific,　Company,　Civic organization,　Governmental agency

    Type：Seminar, workshop

    総務省の最新公表によると、我が国の総人口に占める高齢者の割合は29.1％で、世界一の高齢者大国であり、認知症患者が増え続けている。アルツハイマー型認知症（Alzheimer's disease, AD）は認知症の約7割を占めており、その脳病態には凝集と沈着したアミロイド(A)を主成分とする老人班とTau蛋白質の異常による神経原線維変性に加え、脳内免疫細胞のミクログリア活性化に伴う脳炎症がある。一方、糖尿病など慢性疾患に伴う全身炎症は脳炎症を誘発し、慢性化させ、ADの発症と進行を促進する。歯周病は中高年の8割に発症する口腔慢性炎症として、全身炎症を増大するため、ADへの関与が関心を集めている。
    これまでの臨床研究から、高齢者における重度歯周病の罹患が認知機能低下と正相関すること、AD発症の数年前から血液中のP.gingivalisなど歯周病病原菌に対する抗体価が高くなったこと、歯周病に侵されるAD患者の認知低下は6ヶ月間で6倍低下することが報告され、歯周病がADの発症と進行への関連が示されている。さらに脳組織を用いた研究により、AD脳にP.gingivalisに由来するLPS やジンジパインが検出されている。
    私たちは長年にわたり炎症のADに関与するメカニズムを追究し続け、AD予防開発も明らかにしている。これまでP.gingvalis菌が年齢に依存して １）AD脳病態を誘発し促進すること、２）全身炎症を増大させること、３）脳外でアミロイドβ産生を誘導すること、４）脳外アミロイドβを脳内に輸入させることを明らかにしてきた。本研修会では口腔から多方向にADの発症と進行に関与するメカニズムを解説し、炎症を対象とした認知症の予防開発も紹介する。
    歯周病はADの発症や進行を促進することから、口腔から「炎症軽減」することで、ADの発症や進行を遅らせることが考えられる。20数年の長いスパンで進行するADの病態から、口腔より「炎症制御」をすることで、高齢に連れて増加する認知症の発症と進行を遅らせる現実的な予防アプローチとなり得る。　我が国の「世界一の健康大国」づくりに口腔から貢献することが大いに期待できる。

  • 歯周病と認知症～関与メカニズムから予防対策を考える～

    福岡県築上町  福岡県築上町立西角田小学校  2022.11

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    Audience：General,　Scientific,　Company,　Civic organization,　Governmental agency

    Type：Lecture

  • 歯周病と認知症　～関与メカニズムから予防対策を考える～

    築上町立西角田小学校  2022.11

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    Audience：Infants,　Schoolchildren,　Junior students,　High school students

    Type：Seminar, workshop

  • 歯周病菌による炎症と認知症　研究最前線　〜 医歯連携で認知症予防を実現に 〜

    兵庫県保険医協会神戸支部講演会  神戸  2022.6

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    Audience：General,　Scientific,　Company,　Civic organization,　Governmental agency

    Type：Lecture

  • P.gingivalis 菌アルツハイマー型認知症に関する研究最前線〜 口腔からスローブレイン・エイジング 〜

    愛知学院歯学部同窓会愛知県支部学術講演会  オンライン  2022.2

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    Audience：General,　Scientific,　Company,　Civic organization,　Governmental agency

    Type：Lecture

  • 日本女性科学者の会奨励賞授賞記念公開講演会/歯周病のアルツハイマー型認知症への関与メカニズム解明

    日本女性科学者の会  オンライン開催  2021.9

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    Audience：General,　Scientific,　Company,　Civic organization,　Governmental agency

    Type：Lecture

  • 福岡県歯科保険医協会　市民公開講演会/歯周病と認知症～最新の研究動向～

    福岡県歯科保険医協会  オンライン開催  2021.9

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    Audience：General,　Scientific,　Company,　Civic organization,　Governmental agency

    Type：Lecture

    昨年、歯周病菌が体内に侵入すると認知症の７割を占めるアルツハイマー型認知症の原因物質「アミロイドベータ」の脳への蓄積量が通常の１０倍となるなどのメカニズムを
    九州大学などの研究チームが解明し、日本社会に衝撃を与えました。研究チームのリーダーで、テレビ番組などで研究成果をわかりやすく解説されてきた武洲先生に、「歯周病と認知症」、その最新の研究動向をお話しいただきます。また、九大歯学部の皆さんには、新型コロナウイルスによる感染と重症化を予防するために「口から免疫機能を維持・向上させる」提案をしていただきます。私たち歯科医師にとっても、患者・家族の皆さん、医療・介護の多職種の皆さんと協力し、「歯」「口」と全身の健康との関わりをますます学ぶことが急務となっています。「歯」と「口」から全身の健康を守るために、みんなで意見交換しましょう！！

  • 口腔感染症によるアルツハイマー病の関与メカニズム

    九州大学  オンライン  2021.6

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    Audience：General,　Scientific,　Company,　Civic organization,　Governmental agency

    Type：Seminar, workshop

  • 九州大学アジア・オセアニア研究教育機構セミナー/口腔感染症によるアルツハイマー病の関与メカニズム

    九州大学アジア・オセアニア研究教育機構  オンライン開催  2021.6

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    Audience：General,　Scientific,　Company,　Civic organization,　Governmental agency

    Type：Seminar, workshop

  • 第42回九州口腔衛生学会総会シンポジウム講演　「口腔からアルツハイマー型認知症を考える」 https://ameblo.jp/ksfoh/entry-12608977866.html

    第42回九州口腔衛生学会  オンライン開催  2020.9

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    Audience：General,　Scientific,　Company,　Civic organization,　Governmental agency

    Type：Lecture

  • 九州大学関西同窓会・公開講座

    九州大学関西同窓会  大阪  2019.8

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    Audience：General,　Scientific,　Company,　Civic organization,　Governmental agency

    Type：Lecture

  • 九州大学関西同窓会・公開講座

    九州大学関西同窓会  大阪  2019.8

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    Type：Visiting lecture

    researchmap

  • ～口の中の衛生と健康・認知症～

    福岡女学院大学  福岡市  2019.6

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    Audience：General,　Scientific,　Company,　Civic organization,　Governmental agency

    Type：Lecture

  • 「前を向いて、健やかな人生旅を…」中学生のためのキャリアデザイン啓発事業の一環で「中学生向け出前セミナー～わたしらしい生き方を目指して～」の講師

    福岡市立壱岐中学校  2019.6

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    Audience：Infants,　Schoolchildren,　Junior students,　High school students

    Type：Seminar, workshop

  • ～口の中の衛生と健康・認知症～

    福岡女学院大学  福岡市  2019.6

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    Type：Visiting lecture

    researchmap

  • 口腔ブレインサイエンス：口と脳

    放送大学  放送大学福岡学習センター  2019.5

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    Audience：General,　Scientific,　Company,　Civic organization,　Governmental agency

    Type：Lecture

  • 口腔ブレインサイエンス：口と脳

    放送大学  放送大学福岡学習センター  2019.5

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    Type：Visiting lecture

    researchmap

  • 認知症予防のコツはお口にあり ～口腔ブレインサイエンス～

    宗像ユリックス  宗像ユリックス  2018.6

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    Audience：General,　Scientific,　Company,　Civic organization,　Governmental agency

    Type：Lecture

  • 面接授業　「口腔ブレインサイエイン」

    放送大学・福岡学習センター  放送大学・福岡学習センター  2017.12

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    Audience：General,　Scientific,　Company,　Civic organization,　Governmental agency

    Type：Lecture

    超高齢社会においては、認知症が増えています。近年、全身疾患に関与する口腔慢性炎症性疾患である歯周病は、認知症の増大因子として注目されています。本授業では「口腔ブレインサイエイン」という新理念を取り上げ、口腔から脳をまもる科学的知見ならびに具体的口腔ケアを学びます。

  • 面接授業 「口腔ブレインサイエイン」

    放送大学・福岡学習センター  放送大学・福岡学習センター  2017.12

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    Type：Lecture

    超高齢社会においては、認知症が増えています。近年、全身疾患に関与する口腔慢性炎症性疾患である歯周病は、認知症の増大因子として注目されています。本授業では「口腔ブレインサイエイン」という新理念を取り上げ、口腔から脳をまもる科学的知見ならびに具体的口腔ケアを学びます。

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  • 前を向いて、健やかな人生旅を…

    福岡女学院高校出前講義  2015.11

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    Audience：Infants,　Schoolchildren,　Junior students,　High school students

    Type：Seminar, workshop

  • 前を向いて、健やかな人生旅を…

    福岡女学院高校出前講義  2015.11

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    Type：Seminar, workshop

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  • プロフェッショナルへのキャリア＆ライフパス　～女性研究者・技術者編～

    福岡県男女共同参画センターあすばる・九州大学  　西鉄イン福岡　  2014.6

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    Audience：General,　Scientific,　Company,　Civic organization,　Governmental agency

    Type：Lecture

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Media Coverage

  • テレＱ(TVQ九州放送)の番組「You刊ふくおか」「歯や口と認知症」について番組で研究が紹介された。 TV or radio program

    TVQ九州放送  2023.12

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    テレＱ(TVQ九州放送)の番組「You刊ふくおか」「歯や口と認知症」について番組で研究が紹介された。

  • 女性は要注意！歯周病がアルツハイマー病の原因に「“完熟トマト”が予防に役立つ？」【専門家に聞く】

    働く女性のメディア「CHANTO WEB」　主婦と生活社  2023.5

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    女性は要注意！歯周病がアルツハイマー病の原因に「“完熟トマト”が予防に役立つ？」【専門家に聞く】

  • 教えてヨミドック　歯周病と認知症の関係？　

    夕刊　読売新聞  2023.5

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    教えてヨミドック　歯周病と認知症の関係？

  • 口腔から作る健康長寿 Newspaper, magazine

    健康かながわ 神奈川県予防医学協会  2023.4

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    口腔から作る健康長寿

  • 歯周病菌による炎症と認知症最前線 ～医歯連携で認知症予防を実現へ～ Newspaper, magazine

    兵庫県保健医新聞  2022.11

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    歯周病菌による炎症と認知症最前線 ～医歯連携で認知症予防を実現へ～

  • 「認知症最新研究～その原因と治療」 TV or radio program

    BS12  2022.3

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    「認知症最新研究～その原因と治療」

  • 市民ウエブ講演会「歯科が防ぐ認知症、新型コロナ」 Newspaper, magazine

    福岡県歯科保険医新聞  2021.11

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    市民ウエブ講演会「歯科が防ぐ認知症、新型コロナ」

  • 福岡歯科保健医協会「認知症に焦点」公開ウエブ講演会 Newspaper, magazine

    日本歯科新聞  2021.9

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    福岡歯科保健医協会「認知症に焦点」公開ウエブ講演会

  • 特集　歯科から始めるザ・認知症予防

    NiCO  2021.7

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    特集　歯科から始めるザ・認知症予防

  • 「歯周病による全身炎症で認知症に」ついてインタビュー記事 Newspaper, magazine

    全国保険医新聞  2021.4

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    「歯周病による全身炎症で認知症に」ついてインタビュー記事

  • 今日の健康　歯周病と認知症との関係　リモート出演 TV or radio program

    NHK Eテレ  2021.4

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    今日の健康　歯周病と認知症との関係　リモート出演

  • 三回の放送を行いました（2021年1月3日、10日、17日）1回目は、歯周病と認知症をめぐる最新研究、2回目は、歯周病と認知症、３回目アルツハイマー型認知症のリスク回避のために TV or radio program

    文化放送・ハートリング健康ラジオ～認知症と手をつなごう～  2021.1

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    三回の放送を行いました（2021年1月3日、10日、17日）1回目は、歯周病と認知症をめぐる最新研究、2回目は、歯周病と認知症、３回目アルツハイマー型認知症のリスク回避のために

  • 今やりたい認知症予防策　悪玉中の悪玉「ジンジバリス菌」に要注意 Newspaper, magazine

    週刊朝日  2020.12

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    今やりたい認知症予防策　悪玉中の悪玉「ジンジバリス菌」に要注意

  • 歯周病がアルツハイマー病の原因に、口腔ケアでリスク軽減 Newspaper, magazine

    スポーツ報知、夕刊フジ、ゲンダ 、サンスポ、東京中日、東京スポーツ、日刊スポーツ、 デイリー、 スポニチ  2020.12

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    歯周病がアルツハイマー病の原因に、口腔ケアでリスク軽減

  • 「認知症の原因物質　歯周病によって蓄積する仕組みを解明」 https://www.asahi.com/articles/ASNB544G9NB5TIPE003.html Newspaper, magazine

    朝日新聞（2020年10月5日　夕刊・紙面掲載、デジタル版）  2020.10

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    「認知症の原因物質　歯周病によって蓄積する仕組みを解明」
    https://www.asahi.com/articles/ASNB544G9NB5TIPE003.html

  • サンデーライブ　ニュースランキング　6位　認知症原因に”口の病気” TV or radio program

    朝日放送  2020.10

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    サンデーライブ　ニュースランキング　6位　認知症原因に”口の病気”

  • 桜井浩二インサイト　歯周病とアルツハイマー病　電話にて出演 TV or radio program

    RKBラジオ放送  2020.10

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    桜井浩二インサイト　歯周病とアルツハイマー病　電話にて出演

  • 羽鳥慎一モーニングショー　アルツハイマー病原因物質歯周病で脳に蓄積　リモート生出演 TV or radio program

    テレビ朝日  2020.10

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    羽鳥慎一モーニングショー　アルツハイマー病原因物質歯周病で脳に蓄積　リモート生出演

  • 歯周病が認知症を引き起こすおそれ　リモート生解説 TV or radio program

    読売テレビミヤネ屋  2020.10

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    歯周病が認知症を引き起こすおそれ　リモート生解説

  • 朝日放送グッドモーニング　歯周病予防が認知症対策に TV or radio program

    朝日放送  2020.10

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    朝日放送グッドモーニング　歯周病予防が認知症対策に

  • 認知症物質増、歯周病菌が関与 Newspaper, magazine

    日経産業新聞  2019.12

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    認知症物質増、歯周病菌が関与

  • 歯周組織で産生、アルツハイマー病の老人斑成分 Newspaper, magazine

    日本歯科新聞  2019.11

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    歯周組織で産生、アルツハイマー病の老人斑成分

  • 【今年大注目の3つの老化ストップ法】SP 【認知症を予防する科】最新研究で発見！認知症を引き起こす原因物質「LPS」 TV or radio program

    朝日放送  2018.1

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    【今年大注目の3つの老化ストップ法】SP
    【認知症を予防する科】最新研究で発見！認知症を引き起こす原因物質「LPS」

  • 歯周病によるアルツハイマ―原因酵素を特定 Newspaper, magazine

    日本歯科新聞  2017.7

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    歯周病によるアルツハイマ―原因酵素を特定

  • アルツハイマ―歯周病が誘発・九大、関与の酵素特定 Newspaper, magazine

    西日本新聞  2017.7

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    アルツハイマ―歯周病が誘発・九大、関与の酵素特定

  • 歯周病がアルツハイマ―病誘発 Newspaper, magazine

    科学新聞  2017.7

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    歯周病がアルツハイマ―病誘発

  • 神経障害性疼痛解明へ道　九大　慢性化関与の酵素判明 Newspaper, magazine

    読売新聞  2014.2

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    神経障害性疼痛解明へ道　九大　慢性化関与の酵素判明

  • 神経障害性疼痛　酵素が関与　九大チーム　原因特定、治療薬開発へ道 Newspaper, magazine

    西日本新聞  2014.2

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    神経障害性疼痛　酵素が関与　九大チーム　原因特定、治療薬開発へ道

  • 九大、疼痛の原因酵素を特定－新鎮痛剤開発期待 Newspaper, magazine

    日刊工業新聞  2012.8

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    九大、疼痛の原因酵素を特定－新鎮痛剤開発期待

  • リポソーム粒子関節炎の破壊抑制 Newspaper, magazine

    西日本産業新聞  2010.7

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    リポソーム粒子関節炎の破壊抑制

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Acceptance of Foreign Researchers, etc.

  • 中国・浙江大学歯学院

    Acceptance period： 2019.1 - 2019.12   （Period）：1 month or more

    Nationality：China

  • 青海省人民病院

    Acceptance period： 2017.11 - 2018.5  

    Nationality：China

    Business entity：Foreign governments, foreign research institutes, international organizations

  • 中国医科大学歯学部

    Acceptance period： 2016.4 - 2017.2   （Period）：1 month or more

    Nationality：China

  • 青海省人民病院

    Acceptance period： 2015.10 - 2016.3   （Period）：1 month or more

    Nationality：China

  • 中国医科大学・歯学部

    Acceptance period： 2015.3 - 2017.3   （Period）：1 month or more

    Nationality：China

  • 広西省右江民族医学院発生再生分野

    Acceptance period： 2009.5 - 2009.10   （Period）：1 month or more

    Nationality：China

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Travel Abroad

  • 2023.6

    Staying countory name 1：China   Staying institution name 1：紹興文理学院医学院

    Staying institution name 2：吉林大学口腔医学院

  • 2019.9

    Staying countory name 1：China   Staying institution name 1：吉林大学

  • 2017.11

    Staying countory name 1：China   Staying institution name 1：北理工大学

  • 2017.4

    Staying countory name 1：China   Staying institution name 1：深圳職業学院

  • 2017.2

    Staying countory name 1：United Kingdom   Staying institution name 1：University of Southampton

  • 2016.3

    Staying countory name 1：China   Staying institution name 1：吉林大学・歯学部

  • 2016.2

    Staying countory name 1：Japan   Staying institution name 1：中国医科大学・歯学部

  • 2015.12

    Staying countory name 1：China   Staying institution name 1：北京理工大学・生命学院

  • 2015.8

    Staying countory name 1：China   Staying institution name 1：青海人民病院・玉樹チベット州立病院

  • 2015.6 - 2016.6

    Staying countory name 1：China   Staying institution name 1：深圳龍崗中央病院

  • 2015.5

    Staying countory name 1：China   Staying institution name 1：吉林大学

  • 2014.8 - 2015.8

    Staying countory name 1：China   Staying institution name 1：青海省人民病院

  • 2013.3

    Staying countory name 1：China   Staying institution name 1：吉林大学歯学部

  • 2012.8 - 2015.8

    Staying countory name 1：China   Staying institution name 1：青海省人民病院

  • 2012.3

    Staying countory name 1：China   Staying institution name 1：吉林大学歯学部

  • 2011.4 - 2015.6

    Staying countory name 1：Canada   Staying institution name 1：ブリティッシュコロンビア大学

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