Reduced expression of endogenous secretory receptor for advanced glycation endproducts in hippocampal neurons of Alzheimer's disease brains

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著者

    • NOZAKI Ichiro
    • Department of Biochemistry and Molecular Vascular Biology, Kanazawa University Graduate School of Medical Science
    • WATANABE Takuo
    • Department of Biochemistry and Molecular Vascular Biology, Kanazawa University Graduate School of Medical Science
    • TSUNEYAMA Koichi
    • First Department of Pathology, School of Medicine, University of Toyama
    • YAMAMOTO Yasuhiko
    • Department of Biochemistry and Molecular Vascular Biology, Kanazawa University Graduate School of Medical Science
    • OHE Kazuyo
    • Department of Biochemistry and Molecular Vascular Biology, Kanazawa University Graduate School of Medical Science
    • YONEKURA Hideto
    • Department of Biochemistry, Kanazawa Medical University, School of Medicine
    • YAMADA Masahito
    • Department of Neurology and Neurobiology of Aging, Kanazawa University Graduate School of Medical Science
    • YAMAMOTO Hiroshi
    • Department of Biochemistry and Molecular Vascular Biology, Kanazawa University Graduate School of Medical Science

抄録

The receptor for advanced glycation endproducts (RAGE) is a cell-surface multiligand receptor, which interacts with amyloid β (Aβ), a key protein in Alzheimer's disease (AD). RAGE-Aβ interaction is thought to be associated with pathological progression in AD. A splice variant of RAGE, endogenous secretory RAGE (esRAGE) can act as a decoy receptor for RAGE ligands that would prevent the progression of some pathologic conditions. In this study, the expression of esRAGE in the hippocampal tissues from AD brains compared with control (non-AD) was examined by immunohistochemistry and Western blot analysis. Semiquantitative immunohistochemical analysis of hippocampal tissues using esRAGE-specific antibody revealed significantly decreased immunoreactivities in pyramidal cells in CA1 and CA3 regions of AD compared with non-AD. On the other hand, immunoreactivities of astrocytes for esRAGE significantly increased in those regions. Dentate granule cells and astrocytes showed essentially invariant immunoreactivities between AD and non-AD. Changes in esRAGE immunoreactivity in CA3 neurons and astrocytes were observed from the early pathological stages. Moreover, the esRAGE-immunoreactive bands of AD samples were weaker than those of non-AD samples in Western blot analysis. The results indicate that low expression of esRAGE in the hippocampus would be associated with the development of AD.

収録刊行物

  • Archives of histology and cytology

    Archives of histology and cytology 70(5), 279-290, 2007-12-01

    国際組織細胞学会

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各種コード

  • NII論文ID(NAID)
    10021186902
  • NII書誌ID(NCID)
    AA1068990X
  • 本文言語コード
    ENG
  • 資料種別
    ART
  • ISSN
    09149465
  • データ提供元
    CJP書誌  IR  J-STAGE 
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