Shinji Higashi

Summary

Country: Japan

Publications

  1. ncbi Tau accumulation in the nucleus accumbens in tangle-predominant dementia
    Ito Kawakami
    Dementia Research Project, Tokyo Metropolitan Institute of Medical Science, 2 1 6 Kamikitazawa, Setagaya Ku, Tokyo 156 8506, Japan
    Acta Neuropathol Commun 2:40. 2014
  2. ncbi TDP-43 associates with stalled ribosomes and contributes to cell survival during cellular stress
    Shinji Higashi
    Department of Degenerative Neurological Diseases, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo, Japan
    J Neurochem 126:288-300. 2013
  3. ncbi Localization of MAP1-LC3 in vulnerable neurons and Lewy bodies in brains of patients with dementia with Lewy bodies
    Shinji Higashi
    PET CT Dementia Research Center, Juntendo Tokyo Koto Geriatric Medical Center, Juntendo University School of Medicine, Shinsuna, Koto ku, Tokyo, Japan
    J Neuropathol Exp Neurol 70:264-80. 2011
  4. ncbi Neuropathological investigation of the hypometabolic regions on positron emission tomography with [18F] fluorodeoxyglucose in patients with dementia with Lewy bodies
    Koji Kasanuki
    PET CT Dementia Research Center, Juntendo Tokyo Koto Geriatric Medical Center, Juntendo University School of Medicine, 3 3 20 Shinsuna, Tokyo 136 0075, Japan
    J Neurol Sci 314:111-9. 2012
  5. pmc Abnormal localization of leucine-rich repeat kinase 2 to the endosomal-lysosomal compartment in lewy body disease
    Shinji Higashi
    PET CT Dementia Research Center, Juntendo Tokyo Koto Geriatric Medical Center, Juntendo University School of Medicine, Koto ku, Tokyo, Japan
    J Neuropathol Exp Neurol 68:994-1005. 2009
  6. ncbi Distribution of cerebral amyloid deposition and its relevance to clinical phenotype in Lewy body dementia
    Hiroshige Fujishiro
    PET CT Dementia Research Center, Juntendo Tokyo Koto Geriatric Medical Center, Juntendo University School of Medicine, Koto ku, Tokyo 136 0075, Japan
    Neurosci Lett 486:19-23. 2010
  7. ncbi Concurrence of TDP-43, tau and alpha-synuclein pathology in brains of Alzheimer's disease and dementia with Lewy bodies
    Shinji Higashi
    Department of Psychiatry, Juntendo Tokyo Koto Geriatric Medical Center, Juntendo University School of Medicine, Tokyo, Japan
    Brain Res 1184:284-94. 2007
  8. ncbi Diffuse occipital hypometabolism on [18 F]-FDG PET scans in patients with idiopathic REM sleep behavior disorder: prodromal dementia with Lewy bodies?
    Hiroshige Fujishiro
    PET CT Dementia Research Center, Juntendo Tokyo Koto Geriatric Medical Center, Juntendo University School of Medicine, Tokyo, Japan
    Psychogeriatrics 10:144-52. 2010
  9. ncbi GIGYF2 is present in endosomal compartments in the mammalian brains and enhances IGF-1-induced ERK1/2 activation
    Shinji Higashi
    Department of Degenerative Neurological Diseases, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Ogawa Higashi, Kodaira shi, Tokyo, Japan
    J Neurochem 115:423-37. 2010
  10. ncbi Localization of fused in sarcoma (FUS) protein to the post-synaptic density in the brain
    Naoya Aoki
    Dementia Project, Department of Dementia and Higher Brain Function, Tokyo Metropolitan Institute of Medical Science, 2 1 6 Kamikitazawa, Setagaya Ku, Tokyo, 156 8506, Japan
    Acta Neuropathol 124:383-94. 2012

Collaborators

Detail Information

Publications14

  1. ncbi Tau accumulation in the nucleus accumbens in tangle-predominant dementia
    Ito Kawakami
    Dementia Research Project, Tokyo Metropolitan Institute of Medical Science, 2 1 6 Kamikitazawa, Setagaya Ku, Tokyo 156 8506, Japan
    Acta Neuropathol Commun 2:40. 2014
    ..TPD is an under-recognized disease, while it is a common cause of dementia in those over 80 years of age. In the present study, we describe hyperphosphorylated tau (tau) accumulation in the nucleus accumbens (Acb) in patients with TPD...
  2. ncbi TDP-43 associates with stalled ribosomes and contributes to cell survival during cellular stress
    Shinji Higashi
    Department of Degenerative Neurological Diseases, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo, Japan
    J Neurochem 126:288-300. 2013
    ..Thus, TDP-43 associates with stalled ribosomes and contributes to cell survival during cellular stress. ..
  3. ncbi Localization of MAP1-LC3 in vulnerable neurons and Lewy bodies in brains of patients with dementia with Lewy bodies
    Shinji Higashi
    PET CT Dementia Research Center, Juntendo Tokyo Koto Geriatric Medical Center, Juntendo University School of Medicine, Shinsuna, Koto ku, Tokyo, Japan
    J Neuropathol Exp Neurol 70:264-80. 2011
    ..These results support apotential role for the autophagy-lysosome pathway in the pathogenesis of DLB...
  4. ncbi Neuropathological investigation of the hypometabolic regions on positron emission tomography with [18F] fluorodeoxyglucose in patients with dementia with Lewy bodies
    Koji Kasanuki
    PET CT Dementia Research Center, Juntendo Tokyo Koto Geriatric Medical Center, Juntendo University School of Medicine, 3 3 20 Shinsuna, Tokyo 136 0075, Japan
    J Neurol Sci 314:111-9. 2012
    ..These findings indicate that the neuropathological bases of the hypometabolic regions in the temporo-parietal association and occipital area in DLB may be AD pathology and Lewy pathology, respectively...
  5. pmc Abnormal localization of leucine-rich repeat kinase 2 to the endosomal-lysosomal compartment in lewy body disease
    Shinji Higashi
    PET CT Dementia Research Center, Juntendo Tokyo Koto Geriatric Medical Center, Juntendo University School of Medicine, Koto ku, Tokyo, Japan
    J Neuropathol Exp Neurol 68:994-1005. 2009
    ..These results suggest that LRRK2 normally localizes to the endosomal-lysosomal compartment within morphologically altered neurons in neurodegenerative diseases, particularly in the brains of patients with LB diseases...
  6. ncbi Distribution of cerebral amyloid deposition and its relevance to clinical phenotype in Lewy body dementia
    Hiroshige Fujishiro
    PET CT Dementia Research Center, Juntendo Tokyo Koto Geriatric Medical Center, Juntendo University School of Medicine, Koto ku, Tokyo 136 0075, Japan
    Neurosci Lett 486:19-23. 2010
    ..These results suggest that amyloid deposition may contribute to the timing of the onset of dementia relative to that of parkinsonism in Lewy body dementia...
  7. ncbi Concurrence of TDP-43, tau and alpha-synuclein pathology in brains of Alzheimer's disease and dementia with Lewy bodies
    Shinji Higashi
    Department of Psychiatry, Juntendo Tokyo Koto Geriatric Medical Center, Juntendo University School of Medicine, Tokyo, Japan
    Brain Res 1184:284-94. 2007
    ..This study will provide a more in-depth understanding of the various pathogenic pathways leading to neurodegenerative disorders...
  8. ncbi Diffuse occipital hypometabolism on [18 F]-FDG PET scans in patients with idiopathic REM sleep behavior disorder: prodromal dementia with Lewy bodies?
    Hiroshige Fujishiro
    PET CT Dementia Research Center, Juntendo Tokyo Koto Geriatric Medical Center, Juntendo University School of Medicine, Tokyo, Japan
    Psychogeriatrics 10:144-52. 2010
    ..However, the significance of particular patterns on [(18) F]-FDG PET scans in prodromal patients with dementia with Lewy bodies (DLB) remains unclear...
  9. ncbi GIGYF2 is present in endosomal compartments in the mammalian brains and enhances IGF-1-induced ERK1/2 activation
    Shinji Higashi
    Department of Degenerative Neurological Diseases, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Ogawa Higashi, Kodaira shi, Tokyo, Japan
    J Neurochem 115:423-37. 2010
    ..In PD brains, GIGYF2 did not localise to Lewy bodies. Our findings indicate a role for GIGYF2 in the regulation of signalling at endosomes, but no contribution of GIGYF2 to the pathogenesis of PD...
  10. ncbi Localization of fused in sarcoma (FUS) protein to the post-synaptic density in the brain
    Naoya Aoki
    Dementia Project, Department of Dementia and Higher Brain Function, Tokyo Metropolitan Institute of Medical Science, 2 1 6 Kamikitazawa, Setagaya Ku, Tokyo, 156 8506, Japan
    Acta Neuropathol 124:383-94. 2012
    ..The increase in Alzheimer's disease (AD) is less remarkable but still significant. The dendritic localization of FUS and its increase in FTLD-TDP and AD may have some implication for the pathophysiology of neurodegenerative diseases...
  11. ncbi Neuropathological investigation of regions responsible for semantic aphasia in frontotemporal lobar degeneration
    Ryoko Yamamoto
    PET CT Dementia Research Center, Juntendo Tokyo Koto Geriatric Medical Center, Juntendo University School of Medicine, Tokyo, Japan
    Dement Geriatr Cogn Disord 27:214-23. 2009
    ..Previous studies have not clarified the regions responsible for semantic aphasia in aPiD, and there have been no reported neuropathological studies concerning its pathomechanism...
  12. ncbi Appearance pattern of TDP-43 in Japanese frontotemporal lobar degeneration with ubiquitin-positive inclusions
    Shinji Higashi
    Department of Psychiatry, Juntendo Tokyo Koto Geriatric Medical Center, Juntendo University School of Medicine, 3 3 20 Shinsuna, Koto ku, Tokyo 136 0075, Japan
    Neurosci Lett 419:213-8. 2007
    ....
  13. ncbi TDP-43 physically interacts with amyotrophic lateral sclerosis-linked mutant CuZn superoxide dismutase
    Shinji Higashi
    Department of Degenerative Neurological Diseases, National Institute of Neuroscience, National Center of Neurology and Psychiatry, 4 1 1 Ogawa Higashi, Kodaira, Tokyo 187 8502, Japan
    Neurochem Int 57:906-13. 2010
    ..Our findings may contribute to the understanding of links among SALS, ALS1 and ALS10...
  14. ncbi Genetic association between SORL1 polymorphisms and Alzheimer's disease in a Japanese population
    Nobuto Shibata
    Department of Psychiatry, Juntendo University School of Medicine, Tokyo, Japan
    Dement Geriatr Cogn Disord 26:161-4. 2008
    ..It has recently been shown that the neuronal sortilin-related receptor (SORL1) plays an important role in the pathogenesis of Alzheimer's disease (AD)...