K Yanagisawa

Summary

Affiliation: University of Tokyo
Country: Japan

Publications

  1. ncbi request reprint GM1 ganglioside-bound amyloid beta-protein in Alzheimer's disease brain
    K Yanagisawa
    Department of Dementia Research, National Institute for Longevity Sciences, Morioka, Obu, Japan
    Neurobiol Aging 19:S65-7. 1998
  2. ncbi request reprint Apolipoprotein E exhibits isoform-specific promotion of lipid efflux from astrocytes and neurons in culture
    M Michikawa
    Department of Dementia Research, National Institute for Longevity Sciences, Obu, Aichi, Japan
    J Neurochem 74:1008-16. 2000
  3. ncbi request reprint Amyloid beta-protein (A beta) associated with lipid molecules: immunoreactivity distinct from that of soluble A beta
    K Yanagisawa
    Department of Dementia Research, National Institute for Longevity Sciences, Morioka, Obu, Japan
    FEBS Lett 420:43-6. 1997
  4. ncbi request reprint Implications of presenilin 1 mutations in Alzheimer's disease
    H Komano
    Department of Dementia Research, National Institute for Longevity Sciences, Aichi, Japan
    Mech Ageing Dev 107:281-98. 1999
  5. ncbi request reprint A novel action of alzheimer's amyloid beta-protein (Abeta): oligomeric Abeta promotes lipid release
    M Michikawa
    Department of Dementia Research, National Institute for Longevity Sciences, Obu, Aichi 474 8522, Japan
    J Neurosci 21:7226-35. 2001
  6. ncbi request reprint 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) causes Akt phosphorylation and morphological changes in intracellular organellae in cultured rat astrocytes
    I Isobe
    Department of Dementia Research, National Institute for Longevity Sciences, Nagoya City University Medical School, Japan
    J Neurochem 77:274-80. 2001

Collaborators

Detail Information

Publications6

  1. ncbi request reprint GM1 ganglioside-bound amyloid beta-protein in Alzheimer's disease brain
    K Yanagisawa
    Department of Dementia Research, National Institute for Longevity Sciences, Morioka, Obu, Japan
    Neurobiol Aging 19:S65-7. 1998
    ..The present results strongly suggest that Abeta binds to a GM1 ganglioside in such a way that the bound Abeta is only recognized by BAN052, of the monoclonal antibodies used in this study...
  2. ncbi request reprint Apolipoprotein E exhibits isoform-specific promotion of lipid efflux from astrocytes and neurons in culture
    M Michikawa
    Department of Dementia Research, National Institute for Longevity Sciences, Obu, Aichi, Japan
    J Neurochem 74:1008-16. 2000
    ..This study suggests that apoE promotes lipid efflux from astrocytes and neurons in an isoform-specific manner and that cell surface HSPGs and/or HSPG-LRP pathway may mediate this apoE-promoted lipid efflux...
  3. ncbi request reprint Amyloid beta-protein (A beta) associated with lipid molecules: immunoreactivity distinct from that of soluble A beta
    K Yanagisawa
    Department of Dementia Research, National Institute for Longevity Sciences, Morioka, Obu, Japan
    FEBS Lett 420:43-6. 1997
    ..In contrast, a control anti-A beta monoclonal antibody does not recognize the A beta bound to these lipid vesicles. These results indicate that A beta associated with lipids has an immunoreactivity distinct from that of soluble A...
  4. ncbi request reprint Implications of presenilin 1 mutations in Alzheimer's disease
    H Komano
    Department of Dementia Research, National Institute for Longevity Sciences, Aichi, Japan
    Mech Ageing Dev 107:281-98. 1999
    ..To date, the site of Abeta42 generation has not been firmly established. Our data provide new information regarding the site of Abeta42 generation mediated by the FAD-linked mutant PS1...
  5. ncbi request reprint A novel action of alzheimer's amyloid beta-protein (Abeta): oligomeric Abeta promotes lipid release
    M Michikawa
    Department of Dementia Research, National Institute for Longevity Sciences, Obu, Aichi 474 8522, Japan
    J Neurosci 21:7226-35. 2001
    ..Our findings indicate that oligomeric Abeta promotes lipid release from neuronal membrane, which may lead to the disruption of neuronal lipid homeostasis and the loss of neuronal function...
  6. ncbi request reprint 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) causes Akt phosphorylation and morphological changes in intracellular organellae in cultured rat astrocytes
    I Isobe
    Department of Dementia Research, National Institute for Longevity Sciences, Nagoya City University Medical School, Japan
    J Neurochem 77:274-80. 2001
    ..Moreover, MTT or other tetrazolium salts could be used as interesting activators of Akt to investigate the mechanism by which Akt or PI(3)K is activated...