Takuya Tatebe
| Faculty of Pharmaceutical Sciences,Department of Pharmaceutical Sciences | Lecturer |
Last Updated :2026/03/31
■Researcher basic information
Research Keyword
■Career
Career
■Research activity information
Award
- Dec. 2016
Society Encouragement Award (Basic Research Category)
Elucidation of the regulatory and activation mechanisms of KLK7, an astrocyte derived Aβ degrading enzyme - Oct. 2015
Best poster award
IDENTIFICATION OF KLK7 AS A NOVEL AMYLOID-beta PEPTIDE-DEGRADING PROTEASE SECRETED FROM ASTROCYTES - Sep. 2015
Biological Pharmaceutical Sciences Division, Pharmaceutical Society of Japan, 14th Young Researchers Pharma and Bio Forum for the Next Generation, Outstanding Presentation Award
Elucidation of the pathological function of KLK7, a novel amyloid-beta-degrading protease derived from astrocytes - Jan. 2015
Grant-in-Aid for Scientific Research on Innovative Areas: “Brain Environmental Science.”, Research Encouragement Award
Identification of kallikrein-related peptidase 7 as a novel amyloid-beta peptide-degrading protease secreted from astrocytic cells
Paper
- GPR120 Signaling Controls Amyloid-β Degrading Activity of Matrix Metalloproteinases.
Kazunori Kikuchi; Takuya Tatebe; Yuki Sudo; Miyabishara Yokoyama; Kiwami Kidana; Yung Wen Chiu; Sho Takatori; Makoto Arita; Yukiko Hori; Taisuke Tomita
The Journal of neuroscience : the official journal of the Society for Neuroscience, 14 Jul. 2021
Alzheimer's disease (AD) is characterized by the extensive deposition of amyloid-β peptide (Aβ) in the brain. Brain Aβ level is regulated by a balance between Aβ production and clearance. The clearance rate of Aβ is decreased in the brains of sporadic AD patients, indicating that the dysregulation of Aβ clearance mechanisms affects the pathologic process of AD. Astrocytes are among the most abundant cells in the brain and are implicated in the clearance of brain Aβ via their regulation of the blood-brain barrier, glymphatic system, and proteolytic degradation. The cellular morphology and activity of astrocytes are modulated by several molecules, including ω3 polyunsaturated fatty acids, such as docosahexaenoic acid, which is one of the most abundant lipids in the brain, via the G protein-coupled receptor GPR120/FFAR4. In this study, we analyzed the role of GPR120 signaling in the Aβ-degrading activity of astrocytes. Treatment with the selective antagonist upregulated the matrix metalloproteinase (MMP) inhibitor-sensitive Aβ-degrading activity in primary astrocytes. Moreover, the inhibition of GPR120 signaling increased the levels of Mmp2 and Mmp14 mRNAs, and decreased the expression levels of tissue inhibitor of metalloproteinases 3 (Timp3) and Timp4, suggesting that GPR120 negatively regulates the astrocyte-derived MMP network. Finally, the intracerebral injection of GPR120-specific antagonist substantially decreased the levels of TBS-soluble Aβ in male AD model mice, and this effect was canceled by the coinjection of an MMP inhibitor. These data indicate that astrocytic GPR120 signaling negatively regulates the Aβ-degrading activity of MMPs.SIGNIFICANCE STATEMENT The level of amyloid β (Aβ) in the brain is a crucial determinant of the development of Alzheimer's disease. Here we found that astrocytes, which are the most abundant cell type in the CNS, harbor degrading activity against Aβ, which is regulated by GPR120 signaling. GPR120 is involved in the inflammatory response and obesity in peripheral organs. However, the pathophysiological role of GPR120 in Alzheimer's disease remains unknown. We found that selective inhibition of GPR120 signaling in astrocytes increased the Aβ-degrading activity of matrix metalloproteases. Our results suggest that GPR120 in astrocytes is a novel therapeutic target for the development of anti-Aβ therapeutics. - Loss of kallikrein-related peptidase 7 exacerbates amyloid pathology in Alzheimer's disease model mice.
Kiwami Kidana; Takuya Tatebe; Kaori Ito; Norikazu Hara; Akiyoshi Kakita; Takashi Saito; Sho Takatori; Yasuyoshi Ouchi; Takeshi Ikeuchi; Mitsuhiro Makino; Takaomi C Saido; Masahiro Akishita; Takeshi Iwatsubo; Yukiko Hori; Taisuke Tomita
EMBO molecular medicine, Mar. 2018
Deposition of amyloid-β (Aβ) as senile plaques is one of the pathological hallmarks in the brains of Alzheimer's disease (AD) patients. In addition, glial activation has been found in AD brains, although the precise pathological role of astrocytes remains unclear. Here, we identified kallikrein-related peptidase 7 (KLK7) as an astrocyte-derived Aβ degrading enzyme. Expression of KLK7 mRNA was significantly decreased in the brains of AD patients. Ablation of Klk7 exacerbated the thioflavin S-positive Aβ pathology in AD model mice. The expression of Klk7 was upregulated by Aβ treatment in the primary astrocyte, suggesting that Klk7 is homeostatically modulated by Aβ-induced responses. Finally, we found that the Food and Drug Administration-approved anti-dementia drug memantine can increase the expression of Klk7 and Aβ degradation activity specifically in the astrocytes. These data suggest that KLK7 is an important enzyme in the degradation and clearance of deposited Aβ species by astrocytes involved in the pathogenesis of AD. - Dysregulated Metabolism of the Amyloid-β Protein and Therapeutic Approaches in Alzheimer Disease.
Kazunori Kikuchi; Kiwami Kidana; Takuya Tatebe; Taisuke Tomita
Journal of cellular biochemistry, Dec. 2017
Amyloid-β protein (Aβ) is the main component of senile plaques in the brains of Alzheimer disease (AD) patients. Aβ is proteolytically derived from amyloid-β precursor protein by β- and γ-secretases. Secreted Aβ is then eliminated from the central nervous system by multiple clearance mechanisms, including phagocytosis, immune responses, and proteolytic degradation. These dynamic metabolic processes, which are referred to as Aβ economy, regulate steady-state brain Aβ levels. Familial AD-linked genetic mutations augment the production and aggregation of Aβ. In contrast, rare genetic variants that reduce Aβ production were protective against AD. Moreover, decreased Aβ clearance has been demonstrated in sporadic AD patients, suggesting that dysregulation of Aβ economy contributes to the development of AD. Thus, several approaches to inhibit the production as well as to enhance the clearance of Aβ have been investigated as potential therapeutics against AD. In this manuscript, we introduce the molecules and cellular mechanisms involved in the regulation of Aβ economy and discuss the current understanding of these processes in the development of therapeutics against AD. J. Cell. Biochem. 118: 4183-4190, 2017. © 2017 Wiley Periodicals, Inc. - Memantine reduces the production of amyloid-β peptides through modulation of amyloid precursor protein trafficking.
Kaori Ito; Takuya Tatebe; Kunimichi Suzuki; Takashi Hirayama; Maki Hayakawa; Hideo Kubo; Taisuke Tomita; Mitsuhiro Makino
European journal of pharmacology, 05 Mar. 2017
Memantine, an uncompetitive glutamatergic N-methyl-D-aspartate (NMDA) receptor antagonist, is widely used as medication for the treatment of Alzheimer's disease (AD). It has been reported that memantine reduces amyloid-β peptide (Aβ) levels in both neuronal cultures and in brains of animal models of AD. However, the underlying mechanism of these effects is unclear. Here we examined the effect of memantine on Aβ production. Memantine was administered to 9-month-old Tg2576 mice, a transgenic mouse model of AD, at 10 or 20mg/kg/day in drinking water for 1 month. Memantine significantly reduced the amounts of both CHAPS-soluble and CHAPS-insoluble Aβ in the brains of Tg2576 mice. Memantine at 10mg/kg/day for 1 month also reduced the levels of insoluble Aβ42 in the brains of aged F344 rats. Moreover, memantine reduced Aβ and sAPPβ levels in conditioned media from rat primary cortical cultures without affecting the enzymatic activities of α-secretase, β-secretase, or γ-secretase. Notably, in a cell-surface biotinylation assay, memantine increased the amount of amyloid precursor protein (APP) at the cell surface without changing the total amount of APP. Collectively, our results indicate that chronic treatment with memantine reduces the levels of Aβ both in AD models and in aged animals, and that memantine affects the endocytosis pathway of APP, which is required for β-secretase-mediated cleavage. This leads to a reduction in Aβ production. These results suggest that memantine reduces Aβ production and plaque deposition through the regulation of intracellular trafficking of APP.
MISC
- Implementation of Virtual Reality in Pharmacology Education: A Pilot Approach to Practical Training Involving Animal Experiments
Takahiro Toda; Takuya Tatebe; Kotaro Takasaki; Takashi Yoshida; Takayuki Yoshida; Mami Kikuchi; Miwako Kamei
Mar. 2025 - Synthesis of 2-phenylbenzofuran BF168 with low toxicity and potent amyloid-β aggregation inhibitory activity and structure determination of unexpected product A
長谷川真子; 建部卓也; 中込広大; 鈴木英治
日本薬学会年会要旨集(Web), 2025 - Induction of anti-tumor immunity by cancer cells expressing BCG antigen with IL-2
建部卓也; 石田功
日本薬学会年会要旨集(Web), Mar. 2021 - 脳疾患におけるグリア病態の新展開 アストロサイト由来アミロイドβ分解酵素KLK7の発現制御機構の解明
Dec. 2017 - 脂質メディエーターによるアミロイドβ分解活性の制御機構解明
Mar. 2017 - アストロサイト由来Aβ分解酵素KLK7の発現制御・活性化機構の解明
Oct. 2016 - アストロサイト由来新規アミロイドβ分解酵素KLK7の病的意義解明
Sep. 2016 - アストロサイト由来新規Aβ分解酵素KLK7の病的機能解明
Mar. 2016 - Aβ除去メカニズムUpdate Degradation/Clearance System of Pathogenic Molecules-Update アストロサイト由来新規Aβ分解酵素KLK7の同定と解析
Sep. 2015 - グリア系培養細胞上清中に含まれるセリンプロテアーゼ様Aβ分解活性の解析
Mar. 2014
Lectures, oral presentations, etc.
Research Themes
- Development of killer T cell-mediated cancer therapeutic vaccine by microbial-derived antigen-expressing cancer cell transplantation
Grant-in-Aid for Early-Career Scientists
Teikyo Heisei University
01 Apr. 2022 - 31 Mar. 2025 - 新型コロナウイルス細胞性免疫誘導型ワクチン開発とHLA発現マウスモデルでの評価
01 Apr. 2022 - 31 Mar. 2025 - Development of cancer treatment vaccine that can cover the majority of Japanese
Grant-in-Aid for Early-Career Scientists
Teikyo Heisei University
01 Apr. 2019 - 31 Mar. 2022
Industrial Property Rights
■Profile Information
■Achievement List
Research Keywords
Career
Most Recent Educational Background
Committee History
Award History
- Young Investigator Symposium on Brain Environment, Grant-in-Aid for Scientific Research on Innovative Areas, Young Researcher Award
Identification of kallikrein-related peptidase 7 as a novel amyloid-beta peptide-degrading protease secreted from astrocytic cells, Jan. 2015, Ministry of Education, Culture, Sports, Science and Technology, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Research Encouragement Award, Japan, We reported the identification of KLK7, an amyloid beta degrading enzyme derived from glial cells in the brain, and analyzed its physiological significance.
oral presentation - 14th Young Researchers Pharma and Bio Forum for the Next Generation, Outstanding Presentation Award
Elucidation of the pathological function of KLK7, a novel amyloid-beta-degrading protease derived from astrocytes, Sep. 2015, Biological Pharmaceutical Sciences Division, Pharmaceutical Society of Japan, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Outstanding Presentation Award, Japan, We identified KLK7 as a protease secreted from astrocytes in the brain that degrades amyloid-beta, a key pathogenic factor in Alzheimer disease, and analyzed its physiological significance before presenting our findings.
oral presentation - 6TH INTERNATIONAL SYMPOSIUM KALLIKREIN AND KALLIKREIN-RELAED PEPTIDASES Best poster award
IDENTIFICATION OF KLK7 AS A NOVEL AMYLOID-beta PEPTIDE-DEGRADING PROTEASE SECRETED FROM ASTROCYTES, Oct. 2015, Institute of Molecular Genetics of the CAS, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Best poster award, Australia, We reported that KLK7, an amyloid-beta-degrading enzyme derived from astrocytes, exhibits functional efficacy in an Alzheimer disease model.
poster presentation - 35th Annual Meeting of the Japanese Society of Dementia Society Encouragement Award (Basic Research Category)
Elucidation of the regulatory and activation mechanisms of KLK7, an astrocyte derived amyloid beta degrading enzyme, Dec. 2016, The Japanese Society for Dementia Research, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Society Encouragement Award (Basic Research Category), Japan, We reported at a conference our findings on how KLK7, an amyloid beta degrading enzyme, is regulated in the brain.
Poster presentation
Paper
- Implementation of Virtual Reality in Pharmacology Education: A Pilot Approach to Practical Training Involving Animal Experiments
Co-authorship, Takahiro Toda, Takuya Tatebe, Kotaro Takasaki, Takashi Yoshida, Takayuki Yoshida, Mami Kikuchi, Miwako Kamei, Conceptualization, Investigation,Data curation, Writing, We introduced VR into third-year animal experiments to address limitations in conventional demonstrations and improve adherence to the 3R principles, enhancing both educational effectiveness and animal welfare., Teikyo Heisei University, Vol.18, No.1, 09, 14, 31 Mar. 2025 - Memantine reduces the production of amyloid-beta peptides through modulation of amyloid precursor protein trafficking.
Co-authorship, Ito, K. Tatebe, T. Suzuki, K. Hirayama, T. Hayakawa, M. Kubo, H. Tomita, T. Makino, M, Conceptualization, Investigation, Data curation, Writing, Memantine has been shown to suppress the production of amyloid beta peptides by modulating the trafficking of amyloid precursor protein (APP). This study suggests its potential to reduce neurotoxicity and slow disease progression in Alzheimers disease., European Journal of Pharmacology, 798, 16, 25, Feb. 2017, English, Research Article, https://doi.org/10.1016/j.ejphar.2017.02.001, https://www.ncbi.nlm.nih.gov/pubmed/28167259 - Dysregulated metabolism of the amyloid-beta protein and therapeutic approaches in Alzheimer disease.
Co-authorship, Kikuchi K, Kidana K, Tatebe T, Tomita T, Conceptualization, Writing, We introduced the molecules and cellular mechanisms involved in the regulation of Abeta economy and discuss the current understanding of these processes in the development of therapeutics against AD., Journal of Cellular Biochemistry, WILEY, 118, 12, 4183, 4190, Dec. 2017, English, Research Article, https://doi.org/10.1002/jcb.26129, https://www.ncbi.nlm.nih.gov/pubmed/28488760 - Loss of astrocyte-derived kallikrein 7 exacerbates amyloid pathology in Alzheimer disease model mouse.
Co-authorship, Kidana K, Tatebe T, Ito K, Saito T, Kikuchi K, Takatori S, Ouchi Y, Saido T, Makino M, Akishita M, Iwatsubo T, Hori Y, Tomita T, Conceptualization, Investigation,Data curation, Writing-Original Draft, Writing-Review & Editing, We identified kallikrein-related peptidase 7 (KLK7) as an astrocyte derived Abeta degrading enzyme. Expression of KLK7 mRNA was significantly decreased in the brains of AD patients. We suggest that KLK7 is an important enzyme in the degradation and clearance of deposited Abeta species by astrocytes involved in the pathogenesis of AD., EMBO Molecular Medicine, WILEY, 10, 3, Mar. 2018, Research Article, https://doi.org/10.15252/emmm.201708184, https://www.ncbi.nlm.nih.gov/pubmed/29311134, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5840542 - GPR120 signaling controls amyloid-beta degrading activity of matrix metalloproteinases
Co-authorship, Kikuchi K, Tatebe T, Sudo Y, Yokoyama M, Kidana K, Chiu Y, Takatori S, Arita M, Hori Y, Tomita T, Conceptualization, Data curation, Writing-Original Draft, Writing-Review & Editing, GPR120 signaling was shown to regulate the amyloid beta degrading activity of matrix metalloproteinases (MMPs). This study suggests that GPR120 mediated signaling may influence amyloid beta metabolism in the brain, highlighting its potential as a novel therapeutic target for Alzheimers disease., Journal of Neuroscience, SOCIETY FOR NEUROSCIENCE, 41, 28, JN, RM, Jun. 2021, Research Article, https://doi.org/10.1523/JNEUROSCI.2595-20.2021, https://www.ncbi.nlm.nih.gov/pubmed/34099509, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8276734
MISC
- Synthesis of 2-phenylbenzofuran BF168 with low toxicity and potent amyloid-beta aggregation inhibitory activity and structure determination of unexpected product A
Co-authorship, We previously identified potent Abeta aggregation inhibitors (160, 170, 174, 168). Cytotoxicity testing in N2a cells showed that compound 168 had the lowest toxicity., 145th
2025
0918-9823
202502253024689435 - Induction of antitumor immunity by cancer cells coexpressing BCG antigens and IL-2
Co-authorship, 141年会, 29P01, 175
Mar. 2021
0918-9823
202102230298940720 - Induction of antitumor immunity by cancer cells expressing BCG antigens
Co-authorship, 64th
2020
202002254717086390 - Analysis of the regulatory mechanisms governing the expression of astrocyte-derived amyloid-beta-degrading enzyme kallikrein-related peptidase 7
Co-authorship, 32, 3, 415, 415
Sep. 2018
1342-646X
201802256069212938 - New Developments in Glial Pathophysiology in Brain Disorders: Elucidation of the Regulatory Mechanisms Governing the Expression of KLK7, an Astrocyte-Derived Amyloid-beta-Degrading Enzyme
Co-authorship, 2017年度, [1AW24, 3]
Dec. 2017 - Elucidation of the regulatory mechanisms of amyloid-beta-degrading activity mediated by lipid mediators
Co-authorship, 137年会, 3, 69, 69
Mar. 2017
0918-9823
201702239010449706 - Elucidation of the regulatory and activation mechanisms of KLK7, an astrocyte-derived Abeta-degrading enzyme
Co-authorship, 30, 4, 534, 534
1342-646X
201702282644732135 - Elucidation of the pathological significance of KLK7, a novel astrocyte-derived amyloid-beta-degrading enzyme
Co-authorship, 89回, [1T17, 319)]
Sep. 2016
201602257266113522 - Elucidation of the pathological functions of KLK7, a novel astrocyte-derived Abeta-degrading enzyme
Co-authorship, We found that KLK7, an amyloid-beta-degrading enzyme secreted by astrocytes, is involved in the pathogenesis of Alzheimers disease, and presented these findings., 136年会, 3, 61, 61
Mar. 2016
0918-9823
201602219615098084 - Update on Abeta Removal Mechanisms: Degradation and Clearance Systems-Identification and Characterization of KLK7, a Novel Astrocyte-Derived Abeta-Degrading Enzyme
Co-authorship, 29, 3, 318, 318
Sep. 2015
1342-646X - Identification and characterization of KLK7, a novel astrocyte-derived Abeta-degrading enzyme
Co-authorship, We identified KLK7 as an amyloid-beta-degrading enzyme secreted by astrocytes, a type of glial cell., 29, 3
2015
1342-646X
201502213498195524 - Analysis of serine protease-like amyloid-beta degrading activity in the supernatant of cultured glial cells
Co-authorship, We clarified that the supernatant of glial cells contains a serine-protease-like enzyme capable of degrading amyloid-beta, and presented these findings., 134年会, 3, 56, 56
Mar. 2014
0918-9823
201402212619521004 - Co-authorship, We implemented a vertically integrated curriculum in biology, pharmacology, and pharmacotherapy to help students overcome difficulties and achieve more efficient, deeper learning.
24 Aug. 2025 - Co-authorship, In this study, we incorporated VR into the 2024 Biological Practice II animal experiments to address these issues, enhance learning effectiveness, and further promote adherence to the 3Rs.
24 Aug. 2025
Lectures, oral presentations, etc.
- Fundamentals, Clinical Aspects, and Characteristics of Vaccines for SARS-CoV-2
Takuya Tatebe, Toukatsu Pharmaceutical Study Group, 10 Jul. 2021, Japan
The novel coronavirus disease (COVID-19), which emerged at the end of 2019, triggered a global pandemic and continues to spread worldwide. To overcome this crisis, the development of therapeutics and vaccines targeting the causative virus, SARS-CoV-2, is essential. In this presentation, I will focus on the currently approved treatments and vaccines, and share ongoing research efforts in Japan as well as around the world. - COVID-19 and Infection Control Measures
Takuya Tatebe, Toukatsu Pharmaceutical Study Group, 11 Jan. 2025, Japan
Since the first cases of COVID-19 were identified in China in December 2019, the virus spread globally within a few months. During the peak of the pandemic, many people adopted mask-wearing, hand hygiene, and vaccination as routine measures, and the pandemic has since subsided. However, COVID-19 continues to be reported, and vigilance remains necessary. In this presentation, we will discuss the current status of viral infection, treatments, new types of vaccines, and infection control measures.
Affiliated academic society
Research and Competitive Funding
- Development of cancer treatment vaccine that can cover the majority of Japanese
Ministry of Education, Culture, Sports, Science and Technology, Grant-in-Aid for Scientific Research, Teikyo Heisei University, 01 Apr. 2019 - 31 Mar. 2022
4160000, 3200000, 960000
We are developing a universal cancer therapeutic vaccine using killer T cells sensitized by the BCG vaccine. Since the majority of the population in Japan has received BCG vaccination, it is assumed that most individuals possess cellular immunity against BCG antigens. In fact, BCG antigen-reactive Th1 cells and killer T cells have been reported in BCG-vaccinated Japanese individuals. In this study, we aim to establish a method in which cancer cells are infected with a recombinant virus to specifically express BCG antigens, thereby enabling pre-existing BCG antigen-reactive killer T cells in the body to target and attack the cancer cells. - Development of killer T cell-mediated cancer therapeutic vaccine by microbial-derived antigen-expressing cancer cell transplantation
Ministry of Education, Culture, Sports, Science and Technology, Grant-in-Aid for Scientific Research, Teikyo Heisei University, 01 Apr. 2022 - 31 Mar. 2024
4680000, 3600000, 1080000
In this study, we aim to demonstrate the efficacy of cancer therapeutic vaccines using antigens presented by HLA-A2 (allele A0201), which is common across multiple ethnicities, and HLA-A24 (allele A2402), which is highly frequent in Asian populations, as well as antigens that strongly induce killer T cells in mouse models, with the ultimate goal of clinical application in humans. - Development of a new coronavirus cell-mediated immunity-induced vaccine and evaluation in an HLA-expressing mouse model
Ministry of education, Grant-in-Aid for Scientific Research(C), Teikyo Heisei University, 01 Apr. 2022 - 31 Mar. 2024
Coinvestigator, Isao Ishida, 4160000, 3200000, 960000
Url, In response to the global pandemic of coronavirus disease 2019 (COVID-19), vaccine development has primarily focused on inducing neutralizing antibodies targeting the spike protein on the viral particles. In this study, we aim to develop vaccines that induce cellular immunity against conserved intracellular viral protein antigens shared among beta-coronaviruses, including SARS-CoV-2 and SARS-CoV. The efficacy of these vaccines will be evaluated using HLA-expressing mouse models designed for cellular immune assessment.
Industrial Property Rights
- Patent, MODIFIED CANCER CELL AND CANCER VACCINE COMPOSITION CONTAINING SAME
TATEBE Takuya, ISHIDA Isao, PCT/JP2025/016891, WO/2025/234450
TEIKYO HEISEI UNIVERSITY
The purpose of the present invention is to provide a cancer vaccine composition effective for treating or preventing cancer. The present invention provides a genetically modified cancer cell comprising: a nucleic acid encoding a cytotoxic T cell-inducing antigen and a nucleic acid encoding IL-2. This genetically modified cancer cell can be used as an active ingredient of a cancer vaccine composition.
Social Contribution Activities
- Lets Think About Dementia
Speaker, Teikyo Heisei University, 2024 Nakano Ward Public Lecture, 10 Nov. 2024, Teikyo Heisei University, Nakano Campus
oral presentation, In this lecture, we will provide an easy to understand explanation of the types, symptoms, and progression of dementia, as well as practical ways to cope in daily life. We will also introduce the latest treatments, preventive measures, and local support systems, helping participants deepen their understanding of dementia and apply this knowledge in their daily lives and family interactions., Citizens, Faculty, and Students - Edit|Instructor|Planning, Tokyo Pharmaceutical Association
Streaming, As part of the Tokyo Pharmaceutical Associations Continuing Education Program, we developed and published learning objectives on the causes and pathophysiology of psychiatric disorders and the scope of pharmacotherapy, along with a training syllabus and e-learning materials., Teachers|Researchers|General
Media Coverage
- Researchers at the University of Tokyo and collaborators have discovered an enzyme that suppresses the causative substance of Alzheimers disease.
Dementia Net, 24 Jan. 2018
We identified a novel enzyme, KLK7, that regulates the brain levels and accumulation rate of amyloid-beta, the causative protein of Alzheimers disease, and elucidated its activation mechanism. - Researchers at the University of Tokyo, Daiichi Sankyo, and others have discovered amyloid beta degrading activity in an enzyme secreted by astrocytes.
Nikkei BioTech, 16 Jan. 2018
We identified KLK7 as an amyloid beta degrading enzyme, secreted by astrocytes in the brain, and found its expression to be reduced in the brains of Alzheimers disease patients. KLK7-deficient mice exhibited increased amyloid accumulation. Furthermore, inhibition of glutamate signaling in astrocytes enhanced KLK7 expression and enzymatic activity, highlighting its potential for the development of novel therapeutic and preventive strategies. - Researchers at the University of Tokyo and others have discovered that astrocytes are involved in the pathogenesis of Alzheimers disease.
Nikkei, 08 Jan. 2018
We identified KLK7 as an amyloid beta degrading enzyme, secreted by astrocytes in the brain, and found its expression to be reduced in the brains of Alzheimers disease patients. KLK7-deficient mice exhibited increased amyloid accumulation. Furthermore, inhibition of glutamate signaling in astrocytes enhanced KLK7 expression and enzymatic activity, highlighting its potential for the development of novel therapeutic and preventive strategies. - Astrocytes Implicated in Alzheimers Disease Pathogenesis
Japan Agency for Medical Research and Development (AMED)
We identified KLK7 as an amyloid beta degrading enzyme, secreted by astrocytes in the brain, and found its expression to be reduced in the brains of Alzheimers disease patients. KLK7-deficient mice exhibited increased amyloid accumulation. Furthermore, inhibition of glutamate signaling in astrocytes enhanced KLK7 expression and enzymatic activity, highlighting its potential for the development of novel therapeutic and preventive strategies.
■University education and qualification information
Qualifications, licenses
- 17 Oct. 2017
Certification for Supervisors of Designated Chemical Substances and Tetraalkyl Lead, Completed the Specialized Training Course for Supervisors of Specified Chemical Substances and Tetraalkyl Lead, acquiring knowledge and skills for the safe handling of chemical substances and effective work management. - 01 Mar. 2013
Pharmacist License, Passed the national examination for pharmacists and obtained a pharmacist license. - 07 Jul. 2017
Organic Solvent Work Supervisor, Completed the Organic Solvent Work Supervisor Training Course, acquiring knowledge and skills related to the safe handling of organic solvents and work management. - 13 Apr. 2021
Class A Hazardous Materials Handler License, Passed the Class A Hazardous Materials Handling Examination and obtained a Class A Hazardous Materials Handling License.
