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柳沢 大治郎

所属部署名神経難病研究センター
職名准教授
 
 
更新日: 17/11/17 10:09

研究者基本情報

氏名

    柳沢 大治郎

所属(マスタ)

  • 神経難病研究センター 准教授

学歴

  • 2003年04月- 2008年03月京都薬科大学大学院 薬学研究科 薬学専攻
  • 1998年04月- 2003年03月京都薬科大学 薬学部

学位

  • 博士(薬学)(京都薬科大学)

所属学協会

    日本薬理学会 , Society for Neuroscience , 日本分子イメージング学会 , 日本認知症学会 , 日本神経科学学会 , 日本組織細胞化学会

経歴

  • 2015年07月- 現在滋賀医科大学(准教授)
  • 2012年04月- 2015年06月滋賀医科大学(助教)
  • 2011年04月- 2012年03月日本学術振興会(特別研究員PD)
  • 2010年04月- 2011年03月滋賀医科大学(非常勤研究員)
  • 2008年07月- 2010年03月科学技術振興機構(JST)(技術員/研究員)
  • 2008年04月- 2008年06月京都薬科大学(21世紀COEプログラム ポスト・ドクター)

研究活動情報

論文

  • Tocotrienol-rich fraction modulates amyloid pathology and improves cognitive function in AβPP/PS1 mice
    Ibrahim NF, Yanagisawa D, Durani LW, Hamezah HS, Damanhuri HA, Wan Ngah WZ, Tsuji M, Kiuchi Y, Ono K, Tooyama I
    Journal of Alzheimer’s Disease 55 597-612 2017年 [査読有り]
  • Effects of a DJ-1-binding compound on spatial learning and memory impairment in a mouse model of Alzheimer's disease
    Kitamura Y, Inden M, Kimoto K, Takata K, Yanagisawa D, Hijioka M, Ashihara K, Tooyama I, Shimohama S, Ariga H
    Journal of Alzheimer’s Disease 55(1) 67-72 2017年 [査読有り]
  • Mitochondrial ferritin affects mitochondria by stabilizing HIF-1α in retinal pigment epithelium: implications for the pathophysiology of age-related macular degeneration
    Wang X, Yang H, Yanagisawa D, Bellier JP, Morino K, Zhao S, Liu P, Vigers P, Tooyama I
    Neurobiology of Aging 47 168-179 2016年11月 [査読有り]
  • Fluorodopa is a promising fluorine-19 MRI probe for evaluating striatal dopaminergic function in a rat model of Parkinson's disease
    Yanagisawa D, Oda K, Inden M, Morikawa S, Inubushi T, Taniguchi T, Hijioka M, Kitamura Y, Tooyama I
    Journal of Neuroscience Research 2016年10月 [査読有り]
  • Amyloid imaging using fluorine-19 magnetic resonance imaging (19F-MRI)
    Tooyama I, Yanagisawa D, Taguchi H, Kato T, Hirao K, Shirai N, Sogabe T, Ibrahim NF, Inubushi T, Morikawa S
    Ageing Research Reviews 30 85-94 2016年09月 [査読有り]
  • Taste detection and recognition thresholds in Japanese patients with Alzheimer-type dementia
    Ogawa T, Irikawa N, Yanagisawa D, Shiino A, Tooyama I, Shimizu T
    Auris Nasus Larynx 2016年07月 [査読有り]
  • α4 Nicotinic acetylcholine receptor modulated by galantamine on nigrostriatal terminals regulates dopamine receptor-mediated rotational behavior
    Inden M, Takata K, Yanagisawa D, Ashihara E, Tooyama I, Shimohama S, Kitamura Y
    Neurochemistry International 94 74-81 2016年03月 [査読有り]
  • Therapeutic effects of mesenchymal stem cells for Parkinson’s disease
    Inden M, Yanagisawa D, Hijioka M, Kitamura Y
    Annals of Neurodegenerative Disorders 1 1002 2016年 [査読有り]
  • Curcumin derivative with the substitution at C-4 position, but not curcumin, is effective against amyloid pathology in APP/PS1 mice
    Yanagisawa D, Ibrahim NF, Taguchi H, Morikawa S, Hirao K, Shirai N, Sogabe T, Tooyama I
    Neurobiology of Aging 36(1) 201-210 2015年01月 [査読有り]
  • Up-regulation of mitochondrial ferritin by proinflammatory cytokines: Implications for a role in Alzheimer’s disease
    Yang H, Guan H, Yang M, Liu Z, Takeuchi S, Yanagisawa D, Vincent SR, Zhao S, Tooyama I
    Journal of Alzheimer’s Disease 45(3) 797-811 2015年 [査読有り]
  • Inhalable curcumin: offering the potential for translation to imaging and treatment of Alzheimer’s disease
    McClure R, Yanagisawa D, Stec D, Koktysh D, Xhillari D, Jaeger R, Chekmenev E, Tooyama I, Gore JC, Pham W
    Journal of Alzheimer’s Disease 44(1) 283-295 2015年 [査読有り]
  • Synthesis and tautomerism of curcumin derivatives and related compounds
    Taguchi H, Yanagisawa D, Morikawa S, Hirao K, Shirai N, Tooyama I
    Australian Journal of Chemistry 68 224-229 2015年 [査読有り]
  • Novel curcumin derivatives as potent inhibitors of amyloid β aggregation
    Yanagisawa D, Taguchi H, Morikawa S, Kato T, Hirao K, Shirai N, Tooyama I
    Biochemistry and Biophysics Reports 4 357-368 2015年 [査読有り]
  • A mutation of COX6A1 causes a recessive axonal or mixed form of Charcot-Marie-Tooth disease
    Tamiya G, Makino S, Hayashi M, Abe A, Numakura C, Ueki M, Tanaka A, Ito C, Toshimori K, Ogawa N, Terashima T, Maegawa H, Yanagisawa D, Tooyama I, Tada M, Onodera O, Hayasaka K
    American Journal of Human Genetics 95(3) 294-300 2014年09月 [査読有り]
  • Curcuminoid binds to amyloid β (1-42) oligomer and fibril
    Yanagisawa D, Taguchi H, Yamamoto A, Shirai N, Hirao K, Tooyama I
    Journal of Alzheimer’s Disease 24 Supplement 2 33-42 2014年 [査読有り]
  • Development of a method to measure Aβ42 in nasal cavity samples and its application in normal human volunteers
    Nanjo T, Fukuhara T, Kameshima N, Yanagisawa D, Shimizu S, Shimizu T, Shiino A, Akatsu H, Yamamoto T, Tooyama I
    Journal of Brain Science 44 5-23 2014年 [査読有り]
  • Preferred features of a fluorine-19 MRI probe for amyloid detection in the brain
    Yanagisawa D, Taguchi H, Ibrahim NF, Morikawa S, Shiino A, Inubushi T, Hirao K, Shirai N, Sogabe T, Tooyama I
    Journal of Alzheimer’s Disease 39(3) 617-631 2014年 [査読有り]
  • Mitochondrial ferritin in neurodegenerative diseases
    Yang H, Yang M, Guan H, Liu Z, Zhao S, Takeuchi S, Yanagisawa D, Tooyama I
    Neuroscience Research 77(1-2) 1-7 2013年09月 [査読有り]
  • β-Amyloid peptide (1-40) in the brain reaches the nasal cavity via a non-blood pathway
    Kameshima N, Yanagisawa D, Tooyama I
    Neuroscience Research 76(3) 169-172 2013年07月 [査読有り]
  • Correlation of Aβ deposition in the nasal cavity with the formation of senile plaques in the brain of a transgenic mouse model of Alzheimer's disease
    Kameshima N, Nanjou T, Fukuhara T, Yanagisawa D, Tooyama I
    Neuroscience Letters 513(2) 166-169 2012年04月 [査読有り]
  • In vivo detection of amyloid β deposition using 19F magnetic resonance imaging with a 19F-containing curcumin derivative in a mouse model of Alzheimer’s disease
    Yanagisawa D, Amatsubo T, Morikawa S, Taguchi H, Urushitani M, Shirai N, Hirao K, Shiino A, Inubushi T, Tooyama I
    Neuroscience 184 120-127 2011年 [査読有り]
  • Amyloid imaging using high-field magnetic resonance
    Tomone Amatsubo, Tomone Amatsubo, Daijiro Yanagisawa, Daijiro Yanagisawa, Shigehiro Morikawa, Hiroyasu Taguchi, Ikuo Tooyama
    Magnetic Resonance in Medical Sciences 9 95-99 2010年12月
    The formation of senile plaques followed by deposition of amyloid β peptides (Aβ) are the earliest pathological changes of Alzheimer's disease (AD); thus, detection of the plaques remains the most important early diagnostic indicator of AD. Amyloid imaging is a noninvasive technique for visualizing senile plaques in the brains of patients with Alzheimer's using positron emission tomography (PET) or magnetic resonance (MR) imaging. Several types of probes have been developed for PET, but few ligands have been developed specifically for MR imaging detection of amyloid plaques. This review presents recent advances in amyloid imaging using MR imaging and includes our studies.
  • Relationship between the tautomeric structures of curcumin derivatives and their Aβ-binding activities in the context of therapies for Alzheimer’s disease
    Yanagisawa D, Shirai N, Amatsubo T, Taguchi H, Hirao K, Urushitani M, Morikawa S, Inubushi T, Kato M, Kato F, Morino K, Kimura H, Nakano I, Yoshida C, Okada T, Sano M, Wada Y, Wada KN, Yamamoto A, Tooyama I
    Biomaterials 31(14) 4179-4185 2010年05月 [査読有り]
  • The mRNA distribution of C7orf24, a gamma-glutamyl cyclotransferase, in rat tissues
    Oda K, Makino S, Masuda C, Yoshiki T, Kitamura Y, Takata K, Yanagisawa D, Taniguchi T, Tooyama I
    Journal of Histochemistry & Cytochemistry 57(12) 1121-1126 2009年12月 [査読有り]
  • Oxidative neurodegeneration is prevented by UCP0045037, an allosteric modulator for the reduced form of DJ-1, a wild-type of familial Parkinson’s disease-linked PARK7
    Yamane K, Kitamura Y, Yanagida T, Takata K, Yanagisawa D, Taniguchi T, Taira T, Ariga H
    International Journal of Molecular Sciences 10(11) 4789-4804 2009年11月 [査読有り]
  • Neuroprotective function in brain microglia
    Yoshihisa Kitamura, Daijiro Yanagisawa, Kazuyuki Takata, Takashi Taniguchi
    Current Anaesthesia and Critical Care 20 142-147 2009年06月
    Microglia are uniformly distributed throughout the central nervous system. The number of microglia is thought to make up 5-20% of the entire glial cell population. Origin of microglia has been discussed for several decades. Recently, microglia are widely considered to originate from mesodermal monocyte/macrophage cell lineage, because of similarities in cell surface molecular phenotype. In normal adult brain, microglia have finely branched and ramified cell processes that extend in all directions, and survey the brain microenvironment. When the brain is injured by trauma, stroke and other neurodegenerative disorders, microglia transform their morphology into an activated phenotype, and accumulate in the affected sites. Activation of microglia has been believed to lead to neurotoxic effect, because of results of the in vitro culture studies, which reflects only one possible phenotype of microglia. However, recent studies in the in vivo brain revealed that microglia play a crucial role in neuroprotection against neural cell injury such as cerebral ischemia. Thus, microglial function under pathological conditions in the CNS remains a controversial subject, because of their complexity. In the present review, we summarized the current findings of microglial function, and discussed the possibility of the application to a novel therapeutic strategy. © 2008 Elsevier Ltd. All rights reserved.
  • Protection against oxidative stress-induced neurodegeneration by a modulator for DJ-1, a wild-type of familial Parkinson’s disease-linked PARK7
    Yanagida T, Kitamura Y, Yamane K, Takahashi K, Takata K, Yanagisawa D, Yasui H, Taniguchi T, Taira T, Honda T, Ariga H
    Journal of Pharmacological Sciences 109(3) 463-468 2009年03月 [査読有り]
  • Oxidative stress induction of DJ-1 protein in reactive astrocytes scavenges free radicals and reduces cell injury
    Yanagida T, Tsushima J, Kitamura Y, Yanagisawa D, Takata K, Shibaike T, Yamamoto A, Taniguchi T, Yasui H, Taira T, Morikawa S, Inubushi T, Tooyama I, Ariga H
    Oxidative Medicine and Cellular Longevity 2(1) 36-42 2009年01月 [査読有り]
  • Possible involvement of P2X7 receptor activation in microglial neuroprotection against focal cerebral ischemia in rats
    Yanagisawa D, Kitamura Y, Takata K, Hide I, Nakata Y, Taniguchi T
    Biological & Pharmaceutical Bulletin 31(6) 1121-1130 2008年06月 [査読有り]
  • DJ-1 protects against neurodegeneration caused by focal cerebral ischemia and reperfusion in rats
    Yanagisawa D, Kitamura Y, Inden M, Takata K, Taniguchi T, Morikawa S, Morita M, Inubushi T, Tooyama I, Taira T, Iguchi-Ariga SM, Akaike A, Ariga H
    Journal of Cerebral Blood Flow & Metabolism 28(3) 563-578 2008年03月 [査読有り]
  • Microglial transplantation increases amyloid-beta clearance in Alzheimer model rats
    Takata K, Kitamura Y, Yanagisawa D, Morikawa S, Morita M, Inubushi T, Tsuchiya D, Chishiro S, Saeki M, Taniguchi T, Shimohama S, Tooyama I
    FEBS Letters 581(3) 575-578 2007年02月 [査読有り]
  • PARK7 DJ-1 protects against degeneration of nigral dopaminergic neurons in Parkinson’s disease rat model
    Inden M, Taira T, Kitamura Y, Yanagida T, Tsuchiya D, Takata K, Yanagisawa D, Nishimura K, Taniguchi T, Kiso Y, Yoshimoto K, Agatsuma T, Koide-Yoshida S, Iguchi-Ariga SM, Shimohama S, Ariga H
    Neurobiology of Disease 24(1) 144-158 2006年10月 [査読有り]
  • Improvement of focal ischemia-induced rat dopaminergic dysfunction by striatal transplantation of mouse embryonic stem cells
    Yanagisawa D, Qi M, Kim DH, Kitamura Y, Inden M, Tsuchiya D, Takata K, Taniguchi T, Yoshimoto K, Shimohama S, Akaike A, Sumi S, Inoue K
    Neuroscience Letters 407(1) 74-79 2006年10月 [査読有り]
  • Serofendic acid prevents 6-hydroxydopamine-induced nigral neurodegeneration and drug-induced rotational asymmetry in hemiparkinsonian rats
    Inden M, Kitamura Y, Kondo J, Hayashi K, Yanagida T, Takata K, Tsuchiya D, Yanagisawa D, Nishimura K, Taniguchi T, Shimohama S, Sugimoto H, Akaike A
    Journal of Neurochemistry 95(4) 950-961 2005年11月 [査読有り]
  • Transplantation of mouse embryonic stem cell-derived neurons into the striatum, subthalamic nucleus and substantia nigra, and behavioral recovery in hemiparkinsonian rats
    Inden M, Kim DH, Qi M, Kitamura Y, Yanagisawa D, Nishimura K, Tsuchiya D, Takata K, Hayashi K, Taniguchi T, Yoshimoto K, Shimohama S, Sumi S, Inoue K
    Neuroscience Letters 387(3) 151-156 2005年10月 [査読有り]
  • Recovery of focal brain ischemia-induced behavioral dysfunction by intracerebroventricular injection of microglia.
    Kitamura Y, Yanagisawa D, Inden M, Takata K, Tsuchiya D, Kawasaki T, Taniguchi T, Shimohama S
    Journal of Pharmacological Sciences 97(2) 289-293 2005年02月 [査読有り]
  • Intracerebroventricular injection of microglia protects against focal brain ischemia
    Kitamura Y, Takata K, Inden M, Tsuchiya D, Yanagisawa D, Nakata J, Taniguchi T
    Journal of Pharmacological Sciences 94(2) 203-206 2004年02月 [査読有り]

MISC

  • Curcumin against amyloid pathology in mental health and brain composition
    Ikuo Tooyama, Nor Faeizah Ibrahim, Nor Faeizah Ibrahim, Lina Wati Durani, Lina Wati Durani, Hamizah Shahirah Hamezah, Hamizah Shahirah Hamezah, Mohd Hanafi Ahmad Damanhuri, Wan Zurinah Wan Ngah, Hiroyasu Taguchi, Daijiro Yanagisawa
    Fruits, Vegetables, and Herbs: Bioactive Foods in Health Promotion 487-505 2016年05月
    © 2016 Elsevier Inc. All rights reserved.Recent evidence suggests that amyloid pathology occurs 10-20 years before the clinical onset of Alzheimer's disease (AD). Accordingly, modulating abnormal amyloid-β (Aβ) aggregation is now considered as a potential therapeutic target in AD. Curcumin, a low molecular weight polyphenol derived from the well-known spice turmeric, has various pharmacological properties, including antitumor, antioxidative, antiinflammatory, and antiamyloid effects. Curcumin binds both Aβ fibrils and oligomers and inhibits Aβ aggregation as well as Aβ-related oxidative stress and inflammation. The keto-enol tautomerism of curcumin is involved in its binding to Aβ aggregates. The enol form, but not the keto form, of curcumin can bind to Aβ aggregates. When curcumin was administered to transgenic mouse models of AD, it effectively suppressed amyloid pathology in the mouse brain. However, the results of early clinical trials of curcumin for AD have been negative, probably due to its low bioavailability. Several approaches have been proposed to improve the bioavailability of curcumin.
  • [Glutaminergic neurotransmission in Alzheimer's disease].
    Tooyama I, Yanagisawa D
    Nihon rinsho. Japanese journal of clinical medicine 69 Suppl 8 214-218 2011年10月 [査読有り]

特許

  • ケト・エノール互変異性を利用した診断薬
    特願2009-45531

受賞

  • 2012年11月 第24回日本脳循環代謝学会総会 Young Investigator’s Award
  • 2010年02月 第10回バイオビジネスコンペJAPAN 奨励賞
  • 2008年03月 第81回日本薬理学会年会 年会優秀発表賞