Updated on 2025/09/18

写真a

 
KAWADE Noe
 
Organization
Research Institute of Environmental Medicine Division of Stress Recognition and Response Designated Assistant Professor
Title
Designated Assistant Professor

Degree 1

  1. 博士(農学) ( 2020.3   名古屋大学 ) 

Research History 1

  1. Nagoya University   Designated Assistant Professor

    2021.4

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    Country:Japan

Education 3

  1. Nagoya University

    2017.4 - 2020.3

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    Country: Japan

  2. Nagoya University

    2013.4 - 2015.3

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    Country: Japan

  3. Nagoya University

    2009.4 - 2013.3

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    Country: Japan

Professional Memberships 5

  1. The Japan Neuroscience Society

  2. 日本認知症学会

  3. 日本栄養・食糧学会

  4. 日本農芸化学会

  5. 日本ビタミン学会

Awards 1

  1. 学生優秀発表賞

    2018.5   第72回 日本栄養・食糧学会大会   アスコルビン酸欠乏および不足による肝臓と腸管での炎症関連因子の発現誘導の解析

    川出野絵、鈴木若奈、大谷祥也、小林美里、村井篤嗣、堀尾文彦

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    Award type:Award from Japanese society, conference, symposium, etc.  Country:Japan

 

Papers 13

  1. Microglial cannabinoid receptor type II stimulation improves cognitive impairment and neuroinflammation in Alzheimer's disease mice by controlling astrocyte activation. International journal Open Access

    Akira Sobue, Okiru Komine, Fumito Endo, Chihiro Kakimi, Yuka Miyoshi, Noe Kawade, Seiji Watanabe, Yuko Saito, Shigeo Murayama, Takaomi C Saido, Takashi Saito, Koji Yamanaka

    Cell death & disease   Vol. 15 ( 11 ) page: 858 - 858   2024.11

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

    Alzheimer's disease (AD) is the most common form of dementia and is characterized by the accumulation of amyloid β (Aβ) and phosphorylated tau. Neuroinflammation, mainly mediated by glial activation, plays an important role in AD progression. Although there is growing evidence for the anti-neuroinflammatory and neuroprotective effects of the cannabinoid system modulation, the detailed mechanism remains unclear. To address these issues, we analyzed the expression levels of cannabinoid receptor type II (Cnr2/Cb2) in AppNL-G-F/NL-G-F mice and human AD precuneus, which is vulnerable to amyloid deposition in AD, and the effects of JWH 133, a selective CB2 agonist, on neuroinflammation in primary glial cells and neuroinflammation and cognitive impairment in AppNL-G-F/NL-G-F mice. The levels of Cnr2/Cb2 were upregulated in microglia isolated from the cerebral cortex of AppNL-G-F/NL-G-F mice. CNR2 expression was also increased in RNAs derived from human precuneus with advanced AD pathology. Chronic oral administration of JWH 133 significantly ameliorated the cognitive impairment of AppNL-G-F/NL-G-F mice without neuropsychiatric side effects. Microglia and astrocyte mRNAs were directly isolated from the mouse cerebral cortex by magnetic-activated cell sorting, and the gene expression was determined by quantitative PCR. JWH 133 administration significantly decreased reactive astrocyte markers and microglial C1q, an inducer for the reactive astrocytes in AppNL-G-F/NL-G-F mice. In addition, JWH133 administration inhibited the expression of p-STAT3 (signal transducer and activator of transcription 3) in astrocytes in AppNL-G-F/NL-G-F mice. Furthermore, JWH 133 administration suppressed dystrophic presynaptic terminals surrounding amyloid plaques. In conclusion, stimulation of microglial CB2 ameliorates cognitive dysfunction in AppNL-G-F/NL-G-F mice by controlling astrocyte activation and inducing beneficial neuroinflammation, and our study has implications that CB2 may represent an attractive therapeutic target for the treatment of AD and perhaps other neurodegenerative diseases involving neuroinflammation.

    DOI: 10.1038/s41419-024-07249-6

    Open Access

    Web of Science

    Scopus

    PubMed

  2. Vitamin C deficiency alters the transcriptome of the rat brain in a glucocorticoid-dependent manner, leading to microglial activation and reduced neurogenesis. International journal

    Shunta Goto, Natsuki Kojima, Miyu Komori, Noe Kawade, Kenzi Oshima, Daita Nadano, Nobumitsu Sasaki, Fumihiko Horio, Tsukasa Matsuda, Shinji Miyata

    The Journal of nutritional biochemistry   Vol. 128   page: 109608 - 109608   2024.6

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

    Vitamin C (VitC) is maintained at high concentrations in the brain and is an essential micronutrient for brain function. VitC deficiency leads to neuropsychiatric scurvy, which is characterized by depression and cognitive impairment. However, the molecular mechanism by which mild VitC deficiency impairs brain function is currently unknown. In the present study, we conducted RNA sequencing analysis and found that a short-term VitC deficiency altered the brain transcriptome in ODS rats, which cannot synthesize VitC. Bioinformatic analysis indicated that VitC deficiency affected the expression of genes controlled by the glucocorticoid receptor in the brain. We confirmed an increased secretion of glucocorticoids from the adrenal gland during VitC deficiency. We found that non-neuronal cells, including microglia, which are resident immune cells in the brain, changed their transcriptional patterns in response to VitC deficiency. Immunohistochemical analysis revealed that the quiescent ramified microglia transform into the activated amoeboid microglia during three weeks of VitC deficiency. The morphological activation of microglia was accompanied by increased expression of proinflammatory cytokines such as interleukin-6 in the hippocampus. Furthermore, VitC deficiency decreased the number of newly born neurons in the dentate gyrus of the hippocampus, suggesting that VitC was required for adult neurogenesis that plays a crucial role in learning and memory. Our findings may provide insights into the molecular mechanisms underlying the maintenance of normal brain function by adequate levels of VitC.

    DOI: 10.1016/j.jnutbio.2024.109608

    Web of Science

    Scopus

    PubMed

  3. Genetic background variation impacts microglial heterogeneity and disease progression in amyotrophic lateral sclerosis model mice. International journal Open Access

    Okiru Komine, Syuhei Ohnuma, Kunihiko Hinohara, Yuichiro Hara, Mayuko Shimada, Tomohiro Akashi, Seiji Watanabe, Akira Sobue, Noe Kawade, Tomoo Ogi, Koji Yamanaka

    iScience   Vol. 27 ( 2 ) page: 108872 - 108872   2024.2

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

    Recent single-cell analyses have revealed the complexity of microglial heterogeneity in brain development, aging, and neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS). Disease-associated microglia (DAMs) have been identified in ALS mice model, but their role in ALS pathology remains unclear. The effect of genetic background variations on microglial heterogeneity and functions remains unknown. Herein, we established and analyzed two mice models of ALS with distinct genetic backgrounds of C57BL/6 and BALB/c. We observed that the change in genetic background from C57BL/6 to BALB/c affected microglial heterogeneity and ALS pathology and its progression, likely due to the defective induction of neurotrophic factor-secreting DAMs and impaired microglial survival. Single-cell analyses of ALS mice revealed new markers for each microglial subtype and a possible association between microglial heterogeneity and systemic immune environments. Thus, we highlighted the role of microglia in ALS pathology and importance of genetic background variations in modulating microglial functions.

    DOI: 10.1016/j.isci.2024.108872

    Open Access

    Web of Science

    Scopus

    PubMed

  4. Novel insights into brain lipid metabolism in Alzheimer's disease: Oligodendrocytes and white matter abnormalities. Reviewed International journal Open Access

    Noe Kawade, Koji Yamanaka

    FEBS open bio   Vol. 14 ( 2 ) page: 194 - 216   2024.2

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

    Alzheimer's disease (AD) is the most common cause of dementia. A genome-wide association study has shown that several AD risk genes are involved in lipid metabolism. Additionally, epidemiological studies have indicated that the levels of several lipid species are altered in the AD brain. Therefore, lipid metabolism is likely changed in the AD brain, and these alterations might be associated with an exacerbation of AD pathology. Oligodendrocytes are glial cells that produce the myelin sheath, which is a lipid-rich insulator. Dysfunctions of the myelin sheath have been linked to white matter abnormalities observed in the AD brain. Here, we review the lipid composition and metabolism in the brain and myelin and the association between lipidic alterations and AD pathology. We also present the abnormalities in oligodendrocyte lineage cells and white matter observed in AD. Additionally, we discuss metabolic disorders, including obesity, as AD risk factors and the effects of obesity and dietary intake of lipids on the brain.

    DOI: 10.1002/2211-5463.13661

    Open Access

    Web of Science

    Scopus

    PubMed

  5. Sigma-1 receptor maintains ATAD3A as a monomer to inhibit mitochondrial fragmentation at the mitochondria-associated membrane in amyotrophic lateral sclerosis. Reviewed International journal Open Access

    Seiji Watanabe, Mai Horiuchi, Yuri Murata, Okiru Komine, Noe Kawade, Akira Sobue, Koji Yamanaka

    Neurobiology of disease   Vol. 179   page: 106031 - 106031   2023.4

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

    Organelle contact sites are multifunctional platforms for maintaining cellular homeostasis. Alternations of the mitochondria-associated membranes (MAM), one of the organelle contact sites where the endoplasmic reticulum (ER) is tethered to the mitochondria, have been involved in the pathogenesis of neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS). However, the detailed mechanisms through which MAM integrity is disrupted in ALS have not been fully elucidated. Here, we examined whether AAA ATPase domain-containing protein 3A (ATAD3A), a mitochondrial membrane AAA ATPase accumulating at the MAM, is involved in ALS. We found that sigma-1 receptor (σ1R), an ER-resident MAM protein causative for inherited juvenile ALS, required ATAD3A to maintain the MAM. In addition, σ1R retained ATAD3A as a monomer, which is associated with an inhibition of mitochondrial fragmentation. ATAD3A dimerization and mitochondrial fragmentation were significantly induced in σ1R-deficient or SOD1-linked ALS mouse spinal cords. Overall, these observations indicate that MAM induction by σ1R depends on ATAD3A and that σ1R maintains ATAD3A as a monomer to inhibit mitochondrial fragmentation. Our findings suggest that targeting σ1R-ATAD3A axis would be promising for a novel therapeutic strategy to treat mitochondrial dysfunction in neurological disorders, including ALS.

    DOI: 10.1016/j.nbd.2023.106031

    Open Access

    Web of Science

    Scopus

    PubMed

  6. Low Ascorbic Acid Intake Induces Inflammatory Changes in Intestine and Liver of ODS Rats

    KAWADE Noe, SUZUKI Wakana, KOBAYASHI Misato, OHNO Tamio, MURAI Atsushi, HORIO Fumihiko

    Journal of Nutritional Science and Vitaminology   Vol. 68 ( 6 ) page: 481 - 487   2022.12

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:Center for Academic Publications Japan  

    <p>We previously demonstrated that ascorbic acid (AsA) deficiency, caused by an AsA-free diet, induces inflammatory changes in the liver and intestine of osteogenic disorder Shionogi (ODS) rats that cannot synthesize AsA. However, whether low AsA intake induces inflammatory changes remains unknown. Here, we assessed the inflammatory changes in ODS rats caused by low AsA intake and compared them to ODS rats that were fed a diet supplemented with sufficient amounts of AsA (300 mg/kg). Male ODS rats (12-wk-old) were fed an AsA-free diet (0 ppm group), AsA 20 mg/kg diet (20 ppm group), AsA 40 mg/kg diet (40 ppm group) or AsA 300 mg/kg diet (300 ppm group) for 22 d. The hepatic mRNA levels of acute phase proteins, including C-reactive protein (CRP) and haptoglobin, were higher in the 0 and 20 ppm groups, than in the 300 and 40 ppm groups, but were not significantly higher in the 20 ppm group. Serum CRP concentrations were significantly higher in the 0 and 20 ppm groups than in the 300 and 40 ppm groups. Jejunal and ileal interleukin-1β (IL-1β) mRNA levels were higher in the 0 and 20 ppm groups than in the 300 ppm group. Jejunal and ileal IL-6 mRNA levels tended to be higher in the 0 and 20 ppm groups than in the 300 ppm group. Furthermore, the portal IL-6 concentration gradually increased with decrease in the AsA intake. Thus, inflammatory changes could occur in both AsA-deficient ODS rats and ODS rats with low AsA intake.</p>

    DOI: 10.3177/jnsv.68.481

    Web of Science

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    CiNii Research

  7. アスコルビン酸欠乏は腸内細菌の存在の有無に関わらず肝臓と腸管で炎症関連遺伝子の発現を誘導する

    川出 野絵, 村井 篤嗣, 鈴木 若奈, 竹内 健三郎, 近藤 誠, 小林 美里, 堀尾 文彦

    ビタミン   Vol. 95 ( 3 ) page: 81 - 84   2021.3

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    Language:Japanese   Publisher:公益社団法人 日本ビタミン学会  

    DOI: 10.20632/vso.95.3_81

    CiNii Research

  8. Deficiency of ascorbic acid decreases the contents of tetrahydrobiopterin in the liver and the brain of ODS rats. Reviewed

    Takeshita N., Kawade N., Suzuki W., Hara S., Horio F., Ichinose H.

    Neurosci. Lett.   Vol. 715   page: 134656   2020

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

  9. Ascorbic acid deficiency induces hepatic and intestinal expression of inflammation-related genes irrespective of the presence or absence of gut microbiota in ODS rats. Reviewed

    Kawade N., Murai A., Suzuki W., Takeuchi K., Kondo M., Kobayashi M., Horio F.

    J. Nutr. Biochem.   Vol. 86   page: 108485   2020

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

  10. ビタミンC の疾患に関わる生理機能の解析―抗炎症作用を中心にして―. Reviewed Open Access

    堀尾文彦,川出野絵

    ビタミン   Vol. 94   page: 443   2020

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    Language:Japanese   Publishing type:Research paper (scientific journal)   Publisher:日本ビタミン学会  

    DOI: 10.20632/vso.94.8_443

    Open Access

  11. Ascorbic acid deficiency increases hepatic expression of acute phase proteins through the intestine-derived IL-6 and hepatic STAT3 pathway in ODS rats. Reviewed

    Kawade N., Murai A., Suzuki W., Tokuda Y., Kobayashi M., Horio F.

    J. Nutr. Biochem.   Vol. 70   page: 116   2019

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

  12. アスコルビン酸欠乏は,腸管でのIL-6産生を上昇させて肝臓のSTAT3を活性化することにより急性期タンパク質の発現を上昇させる. Reviewed Open Access

    川出野絵,村井篤嗣,鈴木若奈,徳田優希,小林美里,堀尾文彦

    ビタミン   Vol. 93   page: 485   2019

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    Language:Japanese   Publishing type:Research paper (scientific journal)   Publisher:日本ビタミン学会  

    DOI: 10.20632/vso.93.11_485

    Open Access

  13. Dietary intake of ascorbic acid attenuates lipopolysaccharide-induced sepsis and septic inflammation in ODS rats. Reviewed

    Kawade N., Tokuda Y., Tsujino S., Aoyama H., Kobayashi M., Murai A., Horio F.

    J.Nutr.Sci.Vitaminol.   Vol. 64   page: 404   2018

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

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Books 1

  1. ミクログリアと神経変性疾患(実験医学増刊「シン・マクロ ファージ あらゆる疾患を制御する機能的多様性」)

    川出野絵,山中宏二( Role: Joint author)

    羊土社  2022.3 

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    Responsible for pages:768-773   Language:Japanese

Presentations 22

  1. Evaluation of lipid metabolism in peripheral metabolic organs and brain pathology in Alzheimer's disease model mice fed a high-fat diet.

    2025.7 

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    Event date: 2025.7

    Language:English   Presentation type:Poster presentation  

  2. 肥満時のアルツハイマー病モデルマウスにおける代謝組織での脂質代謝系解析

    川出野絵、小峯起、祖父江顕、齊藤貴志、西道隆臣、山中宏二

    第79回 日本栄養・食糧学会大会  2025.5 

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    Event date: 2025.5

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:名古屋  

  3. 肥満時のアルツハイマー病における脳グリア細胞での脂質代謝系の変動

    川出野絵、小峯起、祖父江顕、齊藤貴志、西道隆臣、山中宏二

    第43回日本認知症学会学術集会  2024.11 

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    Event date: 2024.11

    Language:Japanese   Presentation type:Poster presentation  

    Venue:郡山  

  4. Alterations of lipid profile and gene expressions related to lipid metabolism in the brain of Alzheimer's disease mice.

    2024.7 

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    Event date: 2024.7

    Language:English   Presentation type:Poster presentation  

  5. アルツハイマー病モデルマウスの脳における脂質プロファイルの変化とグリア細胞での脂質代謝系遺伝子発現の変動

    川出野絵、小峯起、祖父江顕、齊藤貴志、西道隆臣、山中宏二

    第78回 日本栄養・食糧学会大会  2024.5 

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    Event date: 2024.5

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:福岡  

  6. 肥満時のアルツハイマー病における脂質代謝系の解析

    川出野絵、小峯起、祖父江顕、齊藤貴志、西道隆臣、山中宏二

    第42回日本認知症学会学術集会  2023.11 

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    Event date: 2023.11

    Language:Japanese   Presentation type:Poster presentation  

    Venue:奈良  

  7. Alteration of brain lipid metabolism in obese Alzheimer's disease model mice.

    2023.8 

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    Event date: 2023.8

    Language:English   Presentation type:Poster presentation  

  8. 肥満時のアルツハイマー病モデルマウスにおける脳と末梢代謝組織での脂質代謝関連因子の解析

    川出野絵、小峯起、祖父江顕、齊藤貴志、西道隆臣、山中宏二

    第77回 日本栄養・食糧学会大会  2023.5 

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    Event date: 2023.5

    Language:Japanese   Presentation type:Poster presentation  

    Venue:札幌  

  9. アルツハイマー病脳における脂質代謝関連因子の遺伝子発現解析

    川出野絵、小峯起、祖父江顕、齊藤貴志、西道隆臣、村山繁雄、山中宏二

    第41回日本認知症学会学術集会 第37回日本老年精神医学会 合同開催  2022.11 

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    Event date: 2022.11

    Language:Japanese   Presentation type:Poster presentation  

    Venue:東京  

  10. アルツハイマー病の患者死後脳とモデルマウス脳における脂質代謝関連因子の解析

    川出野絵、小峯起、祖父江顕、斎藤貴志、西道隆臣、山中宏二

    第76回 日本栄養・食糧学会大会  2022.6 

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    Event date: 2022.6

    Language:Japanese   Presentation type:Oral presentation (general)  

  11. Putative role of altered brain lipid metabolism in Alzheimer's disease pathology using postmortem human brain and mice.

    2022.6 

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    Event date: 2022.6

    Language:English   Presentation type:Poster presentation  

  12. 無菌のODSラットでのアスコルビン酸欠乏時の炎症様変化の解析

    川出野絵、村井篤嗣、鈴木若奈、竹内健三郎、小林美里、堀尾文彦

    日本ビタミン学会 第72回大会  2020.6 

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    Event date: 2020.6

    Language:Japanese   Presentation type:Oral presentation (general)  

  13. 無菌ODS ラットにおけるアスコルビン酸欠乏による腸管と肝臓での炎症様変化の解析

    川出野絵、村井篤嗣、鈴木若奈、竹内健三郎、小林美里、堀尾文彦

    日本農芸化学会 2020年度大会  2020.3 

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    Event date: 2020.3

    Language:Japanese   Presentation type:Oral presentation (general)  

  14. アスコルビン酸欠乏による腸管での炎症様変化と肝臓での急性期タンパク質発現の上昇

    川出野絵、鈴木若奈、小林美里、村井篤嗣、堀尾文彦

    日本ビタミン学会 第71回大会  2019.6  日本ビタミン学会

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    Event date: 2019.6

    Language:Japanese   Presentation type:Oral presentation (general)  

  15. アスコルビン酸欠乏による肝臓での急性期タンパク質発現の上昇と腸管でのサイトカイン発現の上昇

    川出野絵、鈴木若奈、小林美里、村井篤嗣、堀尾文彦

    第73回 日本栄養・食糧学会大会  2019.5  日本栄養・食糧学会

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    Event date: 2019.5

    Language:Japanese   Presentation type:Oral presentation (general)  

  16. アスコルビン酸欠乏時の肝臓でのSTAT3活性化と腸管でのサイトカイン発現の上昇

    川出野絵、鈴木若奈、大谷祥也、小林美里、村井篤嗣、堀尾文彦

    日本ビタミン学会 第70回大会  2018.6 

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    Event date: 2018.6

    Language:Japanese   Presentation type:Oral presentation (general)  

  17. アスコルビン酸欠乏および不足による肝臓と腸管での炎症関連因子の発現誘導の解析

    川出野絵、鈴木若奈、大谷祥也、小林美里、村井篤嗣、堀尾文彦

    第72回 日本栄養・食糧学会大会  2018.5  日本栄養・食糧学会

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    Event date: 2018.5

    Language:Japanese   Presentation type:Oral presentation (general)  

  18. アスコルビン酸欠乏による肝臓と腸管での炎症関連因子の発現誘導

    川出野絵、鈴木若奈、大谷祥也、村井篤嗣、小林美里、堀尾文彦

    日本農芸化学会 2018年度大会  2018.3  日本農芸化学会

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    Event date: 2018.3

    Language:Japanese   Presentation type:Oral presentation (general)  

  19. スコルビン酸欠乏時の肝臓STAT3の活性化と炎症変化

    川出野絵、辻野祥伍、徳田優希、小林美里、村井篤嗣、堀尾文彦

    日本ビタミン学会 第67回大会  2015.6 

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    Event date: 2015.6

    Language:Japanese   Presentation type:Oral presentation (general)  

  20. アスコルビン酸欠乏による肝臓のSTAT3の活性化とその制御下遺伝子の発現解析

    川出野絵、徳田優希、辻野祥伍、小林美里、村井篤嗣、重岡 成、堀尾文彦

    日本農芸化学会 2015年度大会  2015.3  日本農芸化学会

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    Event date: 2015.3

    Language:Japanese   Presentation type:Oral presentation (general)  

  21. アスコルビン酸欠乏時の肝臓でのIL-6、IL-1シグナル系因子の発現上昇と炎症様変化

    川出野絵、徳田優希、辻野祥伍、村井篤嗣、小林美里、堀尾文彦

    日本ビタミン学会 第66回大会  2014.6  日本ビタミン学会

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    Event date: 2014.6

    Language:Japanese   Presentation type:Oral presentation (general)  

  22. アスコルビン酸欠乏による肝臓の転写因子STAT3の活性化とその制御下遺伝子の発現解析

    川出野絵、徳田優希、辻野祥伍、小林美里、村井篤嗣、重岡 成、堀尾文彦

    第68回 日本栄養・食糧学会大会  2014.5  日本栄養・食糧学会

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    Event date: 2014.5

    Language:Japanese   Presentation type:Oral presentation (general)  

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KAKENHI (Grants-in-Aid for Scientific Research) 2

  1. グリア細胞の脂質代謝系に着目した肥満時アルツハイマー病での脳・代謝組織連関の解明

    Grant number:23K13902  2023.4 - 2026.3

    日本学術振興会  科学研究費助成事業  若手研究

    川出 野絵

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    Authorship:Principal investigator 

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

  2. Elucidation of Alzheimer disease pathology in obesity focus on association between brain and other organs and lipid metabolism in glial cells

    Grant number:21K20569  2021.8 - 2024.3

    Grants-in-Aid for Scientific Research  Grant-in-Aid for Research Activity Start-up

    Kawade Noe

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    Authorship:Principal investigator 

    Grant amount:\3120000 ( Direct Cost: \2400000 、 Indirect Cost:\720000 )

 

Teaching Experience (On-campus) 11

  1. 夏休みの研究体験コース

    2025

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    アルツハイマー病モデルマウスの脳での免疫組織化学染色

  2. 「医学入門」基礎医学体験実習

    2025

  3. ベーシックトレーニング(大学院医学基礎実習)

    2024

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    マウス脳からのグリア細胞の初代培養法

  4. 「医学入門」基礎医学体験実習

    2024

  5. 夏休みの研究体験コース

    2024

     詳細を見る

    アルツハイマー病モデルマウスの脳での免疫組織化学染色

  6. ベーシックトレーニング(大学院医学基礎実習)

    2023

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    マウス脳からのグリア細胞の初代培養法

  7. 「医学入門」基礎医学体験実習

    2023

  8. 夏休みの研究体験コース

    2023

     詳細を見る

    アルツハイマー病モデルマウスの脳での免疫組織化学染色

  9. 夏休みの研究体験コース

    2022

     詳細を見る

    アルツハイマー病モデルマウスの脳での免疫組織化学染色

  10. 「医学入門」基礎医学体験実習

    2022

  11. 夏休みの研究体験コース

    2021

     詳細を見る

    アルツハイマー病モデルマウスの脳での免疫組織化学染色

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