Koji Yamanaka

Summary

Affiliation: University of California
Country: USA

Publications

  1. ncbi request reprint Progressive spinal axonal degeneration and slowness in ALS2-deficient mice
    Koji Yamanaka
    Ludwig Institute for Cancer Research and Department of Medicine and Neurosciences, University of California, San Diego, La Jolla, 92093 0670, USA
    Ann Neurol 60:95-104. 2006
  2. pmc Astrocytes as determinants of disease progression in inherited amyotrophic lateral sclerosis
    Koji Yamanaka
    Ludwig Institute for Cancer Research and Department of Medicine and Neuroscience, University of California at San Diego, 9500 Gilman Drive, La Jolla, California 92093 0670, USA
    Nat Neurosci 11:251-3. 2008
  3. pmc Gene transfer demonstrates that muscle is not a primary target for non-cell-autonomous toxicity in familial amyotrophic lateral sclerosis
    Timothy M Miller
    Ludwig Institute for Cancer Research, La Jolla, CA 92093, USA
    Proc Natl Acad Sci U S A 103:19546-51. 2006
  4. pmc Schwann cells expressing dismutase active mutant SOD1 unexpectedly slow disease progression in ALS mice
    Christian S Lobsiger
    Department of Medicine and Neuroscience, Ludwig Institute for Cancer Research, University of California at San Diego, La Jolla, CA 92093, USA
    Proc Natl Acad Sci U S A 106:4465-70. 2009
  5. pmc Misfolded mutant SOD1 directly inhibits VDAC1 conductance in a mouse model of inherited ALS
    Adrian Israelson
    Ludwig Institute for Cancer Research and Department of Cellular and Molecular Medicine, University of California at San Diego, La Jolla, CA 92093 0670, USA
    Neuron 67:575-87. 2010
  6. pmc Mutant dynein (Loa) triggers proprioceptive axon loss that extends survival only in the SOD1 ALS model with highest motor neuron death
    Hristelina S Ilieva
    Ludwig Institute for Cancer Research, University of California at San Diego, La Jolla, CA 92093, USA
    Proc Natl Acad Sci U S A 105:12599-604. 2008
  7. pmc Mutant SOD1 in cell types other than motor neurons and oligodendrocytes accelerates onset of disease in ALS mice
    Koji Yamanaka
    Ludwig Institute for Cancer Research and Department of Medicine and Neuroscience, University of California at San Diego, La Jolla, CA 92093, USA
    Proc Natl Acad Sci U S A 105:7594-9. 2008
  8. ncbi request reprint Onset and progression in inherited ALS determined by motor neurons and microglia
    Severine Boillee
    Ludwig Institute for Cancer Research and Departments of Medicine and Neuroscience, University of California at San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA
    Science 312:1389-92. 2006
  9. pmc Antisense oligonucleotide therapy for neurodegenerative disease
    Richard A Smith
    Ludwig Institute for Cancer Research, University of California, San Diego, La Jolla, California, USA
    J Clin Invest 116:2290-6. 2006
  10. pmc Virus-delivered small RNA silencing sustains strength in amyotrophic lateral sclerosis
    Timothy M Miller
    Ludwig Institute for Cancer Research, University of California, San Diego, USA
    Ann Neurol 57:773-6. 2005

Collaborators

Detail Information

Publications18

  1. ncbi request reprint Progressive spinal axonal degeneration and slowness in ALS2-deficient mice
    Koji Yamanaka
    Ludwig Institute for Cancer Research and Department of Medicine and Neurosciences, University of California, San Diego, La Jolla, 92093 0670, USA
    Ann Neurol 60:95-104. 2006
    ..The goal of this study was to elucidate how the motor system is affected by the deletion of ALS2...
  2. pmc Astrocytes as determinants of disease progression in inherited amyotrophic lateral sclerosis
    Koji Yamanaka
    Ludwig Institute for Cancer Research and Department of Medicine and Neuroscience, University of California at San Diego, 9500 Gilman Drive, La Jolla, California 92093 0670, USA
    Nat Neurosci 11:251-3. 2008
    ..These findings demonstrate that mutant astrocytes are viable targets for therapies for slowing the progression of non-cell autonomous killing of motor neurons in ALS...
  3. pmc Gene transfer demonstrates that muscle is not a primary target for non-cell-autonomous toxicity in familial amyotrophic lateral sclerosis
    Timothy M Miller
    Ludwig Institute for Cancer Research, La Jolla, CA 92093, USA
    Proc Natl Acad Sci U S A 103:19546-51. 2006
    ..Thus, SOD1-mutant-mediated damage within muscles is not a significant contributor to non-cell-autonomous pathogenesis in ALS, and enhancing muscle mass and strength provides no benefit in slowing disease onset or progression...
  4. pmc Schwann cells expressing dismutase active mutant SOD1 unexpectedly slow disease progression in ALS mice
    Christian S Lobsiger
    Department of Medicine and Neuroscience, Ludwig Institute for Cancer Research, University of California at San Diego, La Jolla, CA 92093, USA
    Proc Natl Acad Sci U S A 106:4465-70. 2009
    ..Thus, therapeutic down-regulation of dismutase active mutant SOD1 in familial forms of ALS should be targeted away from Schwann cells...
  5. pmc Misfolded mutant SOD1 directly inhibits VDAC1 conductance in a mouse model of inherited ALS
    Adrian Israelson
    Ludwig Institute for Cancer Research and Department of Cellular and Molecular Medicine, University of California at San Diego, La Jolla, CA 92093 0670, USA
    Neuron 67:575-87. 2010
    ..Taken together, our results establish a direct link between misfolded mutant SOD1 and mitochondrial dysfunction in this form of inherited ALS...
  6. pmc Mutant dynein (Loa) triggers proprioceptive axon loss that extends survival only in the SOD1 ALS model with highest motor neuron death
    Hristelina S Ilieva
    Ludwig Institute for Cancer Research, University of California at San Diego, La Jolla, CA 92093, USA
    Proc Natl Acad Sci U S A 105:12599-604. 2008
    ..These findings support a noncell autonomous, excitotoxic contribution from proprioceptive sensory neurons that modestly accelerates disease onset in inherited ALS...
  7. pmc Mutant SOD1 in cell types other than motor neurons and oligodendrocytes accelerates onset of disease in ALS mice
    Koji Yamanaka
    Ludwig Institute for Cancer Research and Department of Medicine and Neuroscience, University of California at San Diego, La Jolla, CA 92093, USA
    Proc Natl Acad Sci U S A 105:7594-9. 2008
    ..Disease onset is therefore non-cell autonomous, and mutant SOD1 damage within cell types other than motor neurons and oligodendrocytes is a central contributor to initiation of motor neuron degeneration...
  8. ncbi request reprint Onset and progression in inherited ALS determined by motor neurons and microglia
    Severine Boillee
    Ludwig Institute for Cancer Research and Departments of Medicine and Neuroscience, University of California at San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA
    Science 312:1389-92. 2006
    ....
  9. pmc Antisense oligonucleotide therapy for neurodegenerative disease
    Richard A Smith
    Ludwig Institute for Cancer Research, University of California, San Diego, La Jolla, California, USA
    J Clin Invest 116:2290-6. 2006
    ..This suggests that direct delivery of antisense oligonucleotides could be an effective, dosage-regulatable means of treating neurodegenerative diseases, including ALS, where appropriate target proteins are known...
  10. pmc Virus-delivered small RNA silencing sustains strength in amyotrophic lateral sclerosis
    Timothy M Miller
    Ludwig Institute for Cancer Research, University of California, San Diego, USA
    Ann Neurol 57:773-6. 2005
    ....
  11. pmc Gigaxonin controls vimentin organization through a tubulin chaperone-independent pathway
    Don W Cleveland
    Ludwig Institute for Cancer Research, Department of Cellular and Molecular Medicine, University of California at San Diego, La Jolla, CA 92093, USA
    Hum Mol Genet 18:1384-94. 2009
    ..Thus, IF disorganization in GAN fibroblasts is independent of TBCB and microtubule loss and must be regulated by a yet unidentified mechanism...
  12. pmc Unstable mutants in the peripheral endosomal membrane component ALS2 cause early-onset motor neuron disease
    Koji Yamanaka
    Ludwig Institute for Cancer Research and Departments of Medicine and Neuroscience, University of California at San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA
    Proc Natl Acad Sci U S A 100:16041-6. 2003
    ..Thus, mutations in the ALS2 gene linked to early-onset motor neuron disease uniformly produce loss of activity through decreased protein stability of this endosomal GEF...
  13. ncbi request reprint Heat-shock protein 105 interacts with and suppresses aggregation of mutant Cu/Zn superoxide dismutase: clues to a possible strategy for treating ALS
    Hirofumi Yamashita
    Department of Neurology, Kyoto University Graduate School of Medicine, Kyoto, Japan
    J Neurochem 102:1497-505. 2007
    ..Moreover, Hsp105 suppressed the formation of mutant SOD1-containing aggregates in cultured cells. These results suggest that techniques that raise levels of Hsp105 might be promising tools for alleviation of the mutant SOD1 toxicity...
  14. ncbi request reprint Determinants of rapid disease progression in ALS
    Koji Yamanaka
    Neurology 65:1859-60. 2005
  15. ncbi request reprint [ALS and microglia--a player for non-cell-autonomous neuron death]
    Koji Yamanaka
    Yamanaka Research Unit, RIKEN Brain Science Institute, 2 1 Hirosawa, Wako, Saitama 351 0198, Japan
    Brain Nerve 59:1163-70. 2007
    ..In this paper, we review the recent advance of ALS research focusing on the role of glial cells in ALS and discuss its prospect...
  16. ncbi request reprint [Animal models of amyotrophic lateral sclerosis]
    Koji Yamanaka
    Yamanaka Research Unit, RIKEN Brain Science Institute
    Rinsho Shinkeigaku 47:934-7. 2007
    ..In this symposium, I review the recent advance of ALS research focusing on the development of animal models, the role of glial cells in ALS, and therapeutic intervention of rodent models and discuss their prospect...
  17. pmc Complete loss of post-translational modifications triggers fibrillar aggregation of SOD1 in the familial form of amyotrophic lateral sclerosis
    Yoshiaki Furukawa
    Laboratory for Structural Neuropathology, Yamanaka Research Unit, RIKEN Brain Science Institute, Wako, Saitama, Japan
    J Biol Chem 283:24167-76. 2008
    ..Based on our in vivo and in vitro results, we propose that facilitation of post-translational modifications is a promising strategy to reduce SOD1 aggregation in the cell...
  18. ncbi request reprint Novel missense mutation in ALS2 gene results in infantile ascending hereditary spastic paralysis
    Eleonore Eymard-Pierre
    Institut National de la Sante et de la Recherche M├ędicale U384 and Human Genetics Department, CHU, Clermont Ferrand, France
    Ann Neurol 59:976-80. 2006
    ..The goal of this study is to identify novel disease-causing ALS2 mutations...