Y Matsuoka

Summary

Affiliation: Nathan Kline Institute
Country: USA

Publications

  1. ncbi request reprint Novel therapeutic approach for the treatment of Alzheimer's disease by peripheral administration of agents with an affinity to beta-amyloid
    Yasuji Matsuoka
    The Center for Dementia Research, Nathan Kline Institute, Orangeburg, New York 10962, USA
    J Neurosci 23:29-33. 2003
  2. ncbi request reprint Endogenous adenosine protects CA1 neurons from kainic acid-induced neuronal cell loss in the rat hippocampus
    Y Matsuoka
    Department of Neurobiology, Kyoto Pharmaceutical University, Yamashina, Japan
    Eur J Neurosci 11:3617-25. 1999
  3. ncbi request reprint Kainic acid-induced inducible cyclooxygenase and c-Jun phosphorylation in the rat hippocampal formation
    Y Matsuoka
    Department of Neurobiology, Kyoto Pharmaceutical University, Yamashina, Kyoto 607 8412, Japan
    Brain Res 836:213-7. 1999
  4. ncbi request reprint Interferon-gamma plus lipopolysaccharide induction of delayed neuronal apoptosis in rat hippocampus
    Y Matsuoka
    Department of Neurobiology, Kyoto Pharmaceutical University, Yamashina, Japan
    Neurochem Int 34:91-9. 1999
  5. ncbi request reprint Activators of peroxisome proliferator-activated receptor-gamma (PPARgamma) inhibit inducible nitric oxide synthase expression but increase heme oxygenase-1 expression in rat glial cells
    Y Kitamura
    Department of Neurobiology, Kyoto Pharmaceutical University, Japan
    Neurosci Lett 262:129-32. 1999
  6. ncbi request reprint Kainic acid-induced neuronal loss and glial changes in the hippocampal CA3 of p53-deficient mouse
    Y Kitamura
    Department of Neurobiology, Kyoto Pharmaceutical University, Japan
    Neurosci Lett 255:57-60. 1998
  7. ncbi request reprint Induction of plasminogen in rat hippocampal pyramidal neurons by kainic acid
    Y Matsuoka
    Department of Neurobiology, Kyoto Pharmaceutical University, Yamashina, Japan
    Neurosci Lett 252:119-22. 1998
  8. ncbi request reprint Expression of heme oxygenase-1 mediated by non-NMDA and metabotropic receptors in glial cells: possible involvement of reactive oxygen species production and protein kinase C activation
    Y Matsuoka
    Department of Neurobiology, Kyoto Pharmaceutical University, Yamashina, Japan
    Neuropharmacology 38:825-34. 1999
  9. ncbi request reprint Fibrillar beta-amyloid evokes oxidative damage in a transgenic mouse model of Alzheimer's disease
    Y Matsuoka
    Dementia Research Group, Nathan Kline Institute/New York University Medical Center, 140 Old Orangeburg Road, Orangeburg, NY 10962, USA
    Neuroscience 104:609-13. 2001
  10. pmc Inflammatory responses to amyloidosis in a transgenic mouse model of Alzheimer's disease
    Y Matsuoka
    Dementia Research Group, Nathan Kline Institute New York University Medical Center, 14 Old Orangeburg Road, Orangeburg, NY 10462, USA
    Am J Pathol 158:1345-54. 2001

Collaborators

Detail Information

Publications35

  1. ncbi request reprint Novel therapeutic approach for the treatment of Alzheimer's disease by peripheral administration of agents with an affinity to beta-amyloid
    Yasuji Matsuoka
    The Center for Dementia Research, Nathan Kline Institute, Orangeburg, New York 10962, USA
    J Neurosci 23:29-33. 2003
    ....
  2. ncbi request reprint Endogenous adenosine protects CA1 neurons from kainic acid-induced neuronal cell loss in the rat hippocampus
    Y Matsuoka
    Department of Neurobiology, Kyoto Pharmaceutical University, Yamashina, Japan
    Eur J Neurosci 11:3617-25. 1999
    ..These results strongly suggest that endogenous adenosine has neuroprotective effects against excitotoxin-induced neurodegeneration in the CA1 through its A1 receptors...
  3. ncbi request reprint Kainic acid-induced inducible cyclooxygenase and c-Jun phosphorylation in the rat hippocampal formation
    Y Matsuoka
    Department of Neurobiology, Kyoto Pharmaceutical University, Yamashina, Kyoto 607 8412, Japan
    Brain Res 836:213-7. 1999
    ..Almost all of neurons with phosphorylated c-Jun were colocalized with COX-2. These results suggest that COX-2 and c-Jun phosphorylation may participate in KA-induced neurodegeneration...
  4. ncbi request reprint Interferon-gamma plus lipopolysaccharide induction of delayed neuronal apoptosis in rat hippocampus
    Y Matsuoka
    Department of Neurobiology, Kyoto Pharmaceutical University, Yamashina, Japan
    Neurochem Int 34:91-9. 1999
    ..Thus, this animal model may be one of neurodegenerative with extensive inflammatory activation in the hippocampus...
  5. ncbi request reprint Activators of peroxisome proliferator-activated receptor-gamma (PPARgamma) inhibit inducible nitric oxide synthase expression but increase heme oxygenase-1 expression in rat glial cells
    Y Kitamura
    Department of Neurobiology, Kyoto Pharmaceutical University, Japan
    Neurosci Lett 262:129-32. 1999
    ..These results suggest that activation of PPARgamma negatively regulate iNOS expression and positively regulates HO-1 expression in glial cells...
  6. ncbi request reprint Kainic acid-induced neuronal loss and glial changes in the hippocampal CA3 of p53-deficient mouse
    Y Kitamura
    Department of Neurobiology, Kyoto Pharmaceutical University, Japan
    Neurosci Lett 255:57-60. 1998
    ..These observations suggest that p53-null mutation may influence the activation and proliferation of glial cells rather than neuronal death...
  7. ncbi request reprint Induction of plasminogen in rat hippocampal pyramidal neurons by kainic acid
    Y Matsuoka
    Department of Neurobiology, Kyoto Pharmaceutical University, Yamashina, Japan
    Neurosci Lett 252:119-22. 1998
    ..These results suggest that the expression of plasminogen induced by KA-injection may disrupt of neuron-extracellular matrix interaction and thereby contribute to cell death in neurons in the hippocampus...
  8. ncbi request reprint Expression of heme oxygenase-1 mediated by non-NMDA and metabotropic receptors in glial cells: possible involvement of reactive oxygen species production and protein kinase C activation
    Y Matsuoka
    Department of Neurobiology, Kyoto Pharmaceutical University, Yamashina, Japan
    Neuropharmacology 38:825-34. 1999
    ..These results suggest that induction of HO-1 expression by the activation of non-NMDA receptors is mediated by ROS production, and that expression induced by mGluR activation is mediated by PKC activation in rat glial cells...
  9. ncbi request reprint Fibrillar beta-amyloid evokes oxidative damage in a transgenic mouse model of Alzheimer's disease
    Y Matsuoka
    Dementia Research Group, Nathan Kline Institute/New York University Medical Center, 140 Old Orangeburg Road, Orangeburg, NY 10962, USA
    Neuroscience 104:609-13. 2001
    ..From these data we suggest that fibrillar beta-amyloid is associated with oxidative damage which may influence disease progression in the Alzheimer's disease brain...
  10. pmc Inflammatory responses to amyloidosis in a transgenic mouse model of Alzheimer's disease
    Y Matsuoka
    Dementia Research Group, Nathan Kline Institute New York University Medical Center, 14 Old Orangeburg Road, Orangeburg, NY 10462, USA
    Am J Pathol 158:1345-54. 2001
    ....
  11. ncbi request reprint Alteration of transcription factors NF-kappaB and STAT1 in Alzheimer's disease brains
    Y Kitamura
    Department of Neurobiology, Kyoto Pharmaceutical University, Japan
    Neurosci Lett 237:17-20. 1997
    ..These findings suggest that the increased NF-kappaB and STAT1alpha in cell nuclei may be involved in inflammatory activation in AD brains...
  12. ncbi request reprint Protective effects of the antiparkinsonian drugs talipexole and pramipexole against 1-methyl-4-phenylpyridinium-induced apoptotic death in human neuroblastoma SH-SY5Y cells
    Y Kitamura
    Department of Neurobiology, Kyoto Pharmaceutical University, Kyoto 607 8412, Japan
    Mol Pharmacol 54:1046-54. 1998
    ..Pramipexole has similar effects, whereas bromocriptine seems to exhibit the former but not the latter effect...
  13. ncbi request reprint Lack of nigral pathology in transgenic mice expressing human alpha-synuclein driven by the tyrosine hydroxylase promoter
    Y Matsuoka
    Dementia Research Group, Nathan Kline Institute New York University Medical School, 140 Old Orangeburg Road, Orangeburg, New York 10962, USA
    Neurobiol Dis 8:535-9. 2001
    ..These findings suggest that overexpression of alpha-synuclein within nigrostriatal dopaminergic neurons is not in itself sufficient to cause aggregation into Lewy body-like inclusions, nor does it trigger overt neurodegenerative changes...
  14. ncbi request reprint Intermittent fasting and caloric restriction ameliorate age-related behavioral deficits in the triple-transgenic mouse model of Alzheimer's disease
    Veerendra Kumar Madala Halagappa
    Laboratory of Neurosciences, National Institute on Aging, Intramural Research Program, Baltimore, MD 21224, USA
    Neurobiol Dis 26:212-20. 2007
    ..We conclude that CR and IF dietary regimens can ameliorate age-related deficits in cognitive function by mechanisms that may or may not be related to Abeta and tau pathologies...
  15. ncbi request reprint Antibody against C-terminal Abeta selectively elevates plasma Abeta
    Audrey J Gray
    Department of Neurology, Georgetown University Medical Center, Washington, DC 20057, USA
    Neuroreport 18:293-6. 2007
    ..In this study, we found that anti-amyloid beta 40-specific antibody induces amyloid beta sequestration. These results indicate that C-terminal antibodies may be useful in amyloid beta sequestration therapy...
  16. pmc Prophylactic treatment with paroxetine ameliorates behavioral deficits and retards the development of amyloid and tau pathologies in 3xTgAD mice
    Rhonda L Nelson
    Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD, USA
    Exp Neurol 205:166-76. 2007
    ....
  17. ncbi request reprint Intranasal NAP administration reduces accumulation of amyloid peptide and tau hyperphosphorylation in a transgenic mouse model of Alzheimer's disease at early pathological stage
    Yasuji Matsuoka
    Department of Neurology, Georgetown University Medical Center, Washington, DC 20057, USA
    J Mol Neurosci 31:165-70. 2007
    ..Our results indicate that NAP treatment of transgenic mice initiated at an early stage reduced both Abeta and tau pathology, suggesting that NAP might be a potential therapeutic agent for AD...
  18. ncbi request reprint Deglycosylated anti-amyloid beta antibodies reduce microglial phagocytosis and cytokine production while retaining the capacity to induce amyloid beta sequestration
    Kazuyuki Takata
    Department of Neurobiology, Kyoto Pharmaceutical University and 21st Century COE Program, Kyoto 607 8414, Japan
    Eur J Neurosci 26:2458-68. 2007
    ..We conclude that deglycosylated antibodies effectively induced Abeta sequestration without provoking neuroinflammation; thus, these deglycosylated antibodies may be optimal for sequestration therapy for Alzheimer's disease...
  19. doi request reprint A neuronal microtubule-interacting agent, NAPVSIPQ, reduces tau pathology and enhances cognitive function in a mouse model of Alzheimer's disease
    Yasuji Matsuoka
    Department of Neurology, Georgetown University Medical Center, 4000 Reservoir Road N W, Washington, DC 20057, USA
    J Pharmacol Exp Ther 325:146-53. 2008
    ..Our results suggest that neuronal microtubule interacting agents such as NAP may be useful therapeutic agents for the treatment or prevention of tauopathies...
  20. pmc Beta-site amyloid precursor protein-cleaving enzyme-1 (BACE1)-mediated changes of endogenous amyloid beta in wild-type and transgenic mice in vivo
    Chiho Hirata-Fukae
    Department of Neurology, Georgetown University Medical Center, Washington, DC 20057, USA
    Neurosci Lett 435:186-9. 2008
    ..Further, these results suggest that substantial inhibition of BACE1 in brain may be required for clinical benefit in Alzheimer's disease...
  21. ncbi request reprint BACE1 inhibition reduces endogenous Abeta and alters APP processing in wild-type mice
    Kouhei Nishitomi
    Pain and Neurology, Discovery Research Laboratories, Shionogi Co Ltd, Shiga, Japan
    J Neurochem 99:1555-63. 2006
    ..Studies using our new ELISA in non-transgenic mice provide more accurate evaluation of Abeta-reducing strategies than was previously feasible...
  22. ncbi request reprint Presenilin redistribution associated with aberrant cholesterol transport enhances beta-amyloid production in vivo
    Mark Burns
    Center for Dementia Research, Nathan S Kline Institute, Orangeburg, New York 10962, USA
    J Neurosci 23:5645-9. 2003
    ..Our results show that aberrant cholesterol trafficking is associated with the potentiation of APP processing components in vivo, leading to an overall increase in Abeta levels...
  23. ncbi request reprint Organotypic slice cultures from transgenic mice as disease model systems
    Karen Duff
    Nathan Kline Institute and Department of Psychiatry, New York University, 140 Old Orangeburg Rd, Orangeburg, NY 10962, USA
    J Mol Neurosci 19:317-20. 2002
    ..Organotypic slice models are currently being used to test the impact of tangle enhancers or inhibitors as a prescreen for efficacy before testing drugs in vivo...
  24. ncbi request reprint Brain damage results in down-regulation of N-acetylaspartate as a neuronal osmolyte
    Morris H Baslow
    Nathan S Kline Institute for Psychiatric Research, 140 Old Orangeburg Road, Orangeburg, NY 10962, USA
    Neuromolecular Med 3:95-104. 2003
    ..The NAA system, when present in the brain, appears to reflect a high degree of cellular integration, and therefore may be a unique metabolic construct of the intact vertebrate brain...
  25. ncbi request reprint An Abeta sequestration approach using non-antibody Abeta binding agents
    Yasuji Matsuoka
    Department of Neurology, Georgetown University Medical Center, Washington, DC 20057, USA
    Curr Alzheimer Res 2:265-8. 2005
    ..Unfortunately, peripheral administration for three weeks did not substantially alter brain Abeta load. Optimized Abeta binding agents with high affinity to soluble Abeta are necessary for the sequestration approach...
  26. doi request reprint Females exhibit more extensive amyloid, but not tau, pathology in an Alzheimer transgenic model
    Chiho Hirata-Fukae
    Department of Neurology, Georgetown University Medical Center, Washington, DC 20057, USA
    Brain Res 1216:92-103. 2008
    ..These findings confirm progressive Abeta pathology in 3xTg-AD transgenic mice, and provide guidance for their use in therapeutic research...
  27. ncbi request reprint Cdk5 is a key factor in tau aggregation and tangle formation in vivo
    Wendy Noble
    Center for Dementia Research, Nathan S Kline Institute, New York University, 140 Old Orangeburg Road, Orangeburg, NY 10962, USA
    Neuron 38:555-65. 2003
    ..Insoluble tau was also associated with active GSK. Thus, cdk5 can initiate a major impact on tau pathology progression that probably involves several kinases. Kinase inhibitors may thus be beneficial therapeutically...
  28. ncbi request reprint Fyn modulation of Dab1 effects on amyloid precursor protein and ApoE receptor 2 processing
    HYANG SOOK HOE
    Department of Neuroscience, Georgetown University Medical Center, 3970 Reservoir Road NW, Washington, DC 20057, USA
    J Biol Chem 283:6288-99. 2008
    ..These data demonstrate that Fyn, due in part to its effects on Dab1, regulates the phosphorylation, trafficking, and processing of APP and apoEr2...
  29. ncbi request reprint Increased dopaminergic neuron sensitivity to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in transgenic mice expressing mutant A53T alpha-synuclein
    Wai Haung Yu
    Taub Institute on Alzheimer s Disease and Aging, Department of Pathology, Columbia University, Black Bldg 513, 650 W 168th St, New York, NY 10032, USA
    Neurochem Res 33:902-11. 2008
    ..The alpha-syn tg line is therefore useful to study the genetic and environmental inter-relationship in PD...
  30. pmc F-spondin interaction with the apolipoprotein E receptor ApoEr2 affects processing of amyloid precursor protein
    HYANG SOOK HOE
    Department of Neuroscience, Georgetown University Medical Center, 3970 Reservoir Road NW, Washington, DC 20057 1464, USA
    Mol Cell Biol 25:9259-68. 2005
    ..These studies suggest that the extracellular matrix molecule F-spondin can cluster APP and ApoEr2 together on the cell surface and affect the processing of each, resulting in decreased production of Abeta...
  31. ncbi request reprint Development of Abeta terminal end-specific antibodies and sensitive ELISA for Abeta variant
    Yuko Horikoshi
    Immuno biological Laboratories Co, Ltd, Fujioka shi, Gunma 375 0005, Japan
    Biochem Biophys Res Commun 319:733-7. 2004
    ..A combination of C-termini antibodies and an antibody against the middle region of Abeta detects mouse Abeta in non-transgenic mouse brains...
  32. ncbi request reprint Biological significance of isoaspartate and its repair system
    Takahiko Shimizu
    Research Team for Molecular Biomarkers, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan
    Biol Pharm Bull 28:1590-6. 2005
    ..We discuss here the pathological implications of the formation of isoaspartate in damaged proteins during neurodegeneration in model mice and AD...
  33. ncbi request reprint DAB1 and Reelin effects on amyloid precursor protein and ApoE receptor 2 trafficking and processing
    HYANG SOOK HOE
    Department of Neuroscience, Georgetown University Medical Center, Washington, DC 20057 1464, USA
    J Biol Chem 281:35176-85. 2006
    ..Together, these data suggest that Dab1 alters trafficking and processing of APP and apoEr2, and this effect is influenced by extracellular ligands...
  34. ncbi request reprint NAP: research and development of a peptide derived from activity-dependent neuroprotective protein (ADNP)
    Illana Gozes
    Department of Human Molecular Genetics and Biochemistry, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv 69978, Israel
    CNS Drug Rev 11:353-68. 2005
    ..NAP is poised for further clinical development targeting several indications, including Alzheimer's disease...
  35. ncbi request reprint Evidence for peripheral clearance of cerebral Abeta protein following chronic, active Abeta immunization in PSAPP mice
    Cynthia A Lemere
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Neurobiol Dis 14:10-8. 2003
    ..Most of the Abeta in the serum of the immunized mice was bound to antibodies. We conclude that following active immunization, anti-Abeta antibodies sequester serum Abeta and may increase central nervous system to serum Abeta clearance...