F Tanaka

Summary

Affiliation: Nagoya University
Country: Japan

Publications

  1. doi request reprint Neuropathology and omics in motor neuron diseases
    Fumiaki Tanaka
    Department of Neurology, Nagoya University Graduate School of Medicine, Nagoya, Japan
    Neuropathology 32:458-62. 2012
  2. pmc Current status of treatment of spinal and bulbar muscular atrophy
    Fumiaki Tanaka
    Department of Neurology, Nagoya University Graduate School of Medicine, 65 Tsurumai Cho, Showa Ku, Nagoya 466 8550, Japan
    Neural Plast 2012:369284. 2012
  3. doi request reprint Skin biopsy is useful for the antemortem diagnosis of neuronal intranuclear inclusion disease
    J Sone
    Department of Neurology, Nagoya University Graduate School of Medicine, Nagoya, Aichi 466 8550, Japan
    Neurology 76:1372-6. 2011
  4. ncbi request reprint Detection of triplet repeat expansion in the human genome by use of hybridization signal intensity
    K Sawada
    Taisho Laboratory of Functional Genomics, Nara Institute of Science and Technology, Nagoya, Japan
    Anal Biochem 286:59-66. 2000
  5. ncbi request reprint Transforming growth factor-β signaling in motor neuron diseases
    M Katsuno
    Department of Neurology, Nagoya University Graduate School of Medicine, Showa Ku, Nagoya, Japan
    Curr Mol Med 11:48-56. 2011
  6. ncbi request reprint Sisters homozygous for the spinocerebellar ataxia type 6 (SCA6)/CACNA1A gene associated with different clinical phenotypes
    T Kato
    Department of Neurology, Kasugai Municipal Hospital, Japan
    Clin Genet 58:69-73. 2000
  7. ncbi request reprint Cognitive impairment in spinocerebellar ataxia type 6
    M Suenaga
    Department of Neurology, Nagoya University Graduate School of Medicine, 65 Tsurumai cho Showa ku, Nagoya 466 8550 Japan
    J Neurol Neurosurg Psychiatry 79:496-9. 2008
  8. doi request reprint Prefrontal hypoperfusion and cognitive dysfunction correlates in spinocerebellar ataxia type 6
    Y Kawai
    Department of Neurology, Nagoya University Graduate School of Medicine, Nagoya 466 8550, Japan
    J Neurol Sci 271:68-74. 2008
  9. ncbi request reprint Transgenic mice harboring a full-length human mutant DRPLA gene exhibit age-dependent intergenerational and somatic instabilities of CAG repeats comparable with those in DRPLA patients
    T Sato
    Department of Neurology, Brain Research Institute, Niigata University, 1 Asahimachi, Niigata 951 8585, Japan
    Hum Mol Genet 8:99-106. 1999

Collaborators

Detail Information

Publications9

  1. doi request reprint Neuropathology and omics in motor neuron diseases
    Fumiaki Tanaka
    Department of Neurology, Nagoya University Graduate School of Medicine, Nagoya, Japan
    Neuropathology 32:458-62. 2012
    ..Finally, we emphasize the need for creating novel SALS disease models based on the results of omics analysis, especially based on the observation that dynactin-1 gene expression was downregulated in SALS motor neurons...
  2. pmc Current status of treatment of spinal and bulbar muscular atrophy
    Fumiaki Tanaka
    Department of Neurology, Nagoya University Graduate School of Medicine, 65 Tsurumai Cho, Showa Ku, Nagoya 466 8550, Japan
    Neural Plast 2012:369284. 2012
    ..Other treatments targeted for mitochondrial function, ubiquitin-proteasome system (UPS), and autophagy could be applicable for all types of polyglutamine diseases...
  3. doi request reprint Skin biopsy is useful for the antemortem diagnosis of neuronal intranuclear inclusion disease
    J Sone
    Department of Neurology, Nagoya University Graduate School of Medicine, Nagoya, Aichi 466 8550, Japan
    Neurology 76:1372-6. 2011
    ..Because of the variety of clinical manifestations, antemortem diagnosis of NIID is difficult...
  4. ncbi request reprint Detection of triplet repeat expansion in the human genome by use of hybridization signal intensity
    K Sawada
    Taisho Laboratory of Functional Genomics, Nara Institute of Science and Technology, Nagoya, Japan
    Anal Biochem 286:59-66. 2000
    ..The technique has advantages over related techniques because it is more sensitive and can be applied to cases where a small repeat expansion is involved...
  5. ncbi request reprint Transforming growth factor-β signaling in motor neuron diseases
    M Katsuno
    Department of Neurology, Nagoya University Graduate School of Medicine, Showa Ku, Nagoya, Japan
    Curr Mol Med 11:48-56. 2011
    ....
  6. ncbi request reprint Sisters homozygous for the spinocerebellar ataxia type 6 (SCA6)/CACNA1A gene associated with different clinical phenotypes
    T Kato
    Department of Neurology, Kasugai Municipal Hospital, Japan
    Clin Genet 58:69-73. 2000
    ..These findings strongly suggest that the gene dosage influences the age of onset, but other unknown factors are also important in the phenotypic expression of homozygous SCA6...
  7. ncbi request reprint Cognitive impairment in spinocerebellar ataxia type 6
    M Suenaga
    Department of Neurology, Nagoya University Graduate School of Medicine, 65 Tsurumai cho Showa ku, Nagoya 466 8550 Japan
    J Neurol Neurosurg Psychiatry 79:496-9. 2008
    ..The aim of this study was to evaluate cognitive impairment in patients with spinocerebellar ataxia type 6 (SCA6) and to verify the role of cerebellar involvement in intellectual abilities...
  8. doi request reprint Prefrontal hypoperfusion and cognitive dysfunction correlates in spinocerebellar ataxia type 6
    Y Kawai
    Department of Neurology, Nagoya University Graduate School of Medicine, Nagoya 466 8550, Japan
    J Neurol Sci 271:68-74. 2008
    ..The aim of this study is to evaluate the correlation between brain perfusion and cognitive dysfunction in spinocerebellar ataxia type 6 (SCA6) patients...
  9. ncbi request reprint Transgenic mice harboring a full-length human mutant DRPLA gene exhibit age-dependent intergenerational and somatic instabilities of CAG repeats comparable with those in DRPLA patients
    T Sato
    Department of Neurology, Brain Research Institute, Niigata University, 1 Asahimachi, Niigata 951 8585, Japan
    Hum Mol Genet 8:99-106. 1999
    ....