加齢性記憶障害を抑制するDC0遺伝子変異体

DOI
  • 齊藤 実
    (財)東京都医学研究機構・東京都神経科学総合研究所・神経機能分子治療
  • 堀内 純二郎
    (財)東京都医学研究機構・東京都神経科学総合研究所・神経機能分子治療
  • 山崎 大介
    (財)東京都医学研究機構・東京都神経科学総合研究所・神経機能分子治療

書誌事項

タイトル別名
  • The Drosophila DC0 Mutation suppresses age-related memory impairment without affecting lifespan

抄録

Age-related memory impairment (AMI) is one of the most significant phenotype of brain aging and experienced by elderly people even without showing symptoms of age-related neuronal disease such as Alzheimer disease (AD). Identification of genes underlying AMI could light on the molecular mechanisms of AMI and gives clues for therapeutic strategy. However, behavioral genetic for AMI has not been much carried out because of the long lifespan of animal models. Previously, we reported that memory mutant amnesiac (amn) does not show further memory decay upon aging. Since amn encodes neural peptide supposed to control adenylyl cyclase (AC) in mushroom bodies (MBs), neuronal center for memory, we screened mutants of the genes suspected or reported to express in MBs to isolate AMI mutants. Here, we found that heterozygous DC0-PKA mutants (DC0/+) sustain robust young normal memory into old age with no effect on lifespan and its expression level upon aging. Moreover, we found that long-lived mutant does show normal AMI. These findings suggest that DC0-PKA specifically regulate AMI, and extension of longevity is neither essential nor sufficient for suppression of AMI. [J Physiol Sci. 2006;56 Suppl:S221]

収録刊行物

キーワード

詳細情報 詳細情報について

  • CRID
    1390001205727865856
  • NII論文ID
    130005448639
  • DOI
    10.14849/psjproc.2006.0_221_2
  • データソース種別
    • JaLC
    • CiNii Articles
  • 抄録ライセンスフラグ
    使用不可

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