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In search of memory complexes using a BRI2-derived peptide

Research Project

Project/Area Number 16K10209
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Psychiatric science
Research InstitutionGifu University

Principal Investigator

Matsuda Shuji  岐阜大学, 大学院医学系研究科, 准教授 (70296721)

Co-Investigator(Kenkyū-buntansha) 千田 隆夫  岐阜大学, 大学院医学系研究科, 教授 (10187875)
Project Period (FY) 2016-04-01 – 2019-03-31
Project Status Completed (Fiscal Year 2018)
Budget Amount *help
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2018: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2017: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Keywordsアルツハイマー病 / BRi2 / ペプチド / BRI2
Outline of Final Research Achievements

Alzheimer Disease (AD) is the most prevalent dementia in modern societies. The pathogenesis of AD is poorly understood, and its therapies have much room to be improved. Amyloid beta deposits found in the brains of AD patients are processed from the precursor protein of amyloid beta, termed Alzheimer Protein Precursor (APP). We had identified BRI2, which binds and inhibits the processing of APP. This BRI2 inhibits APP processing in cultured cells, and slows the Amyloid beta deposition in AD model mice.
In this research we focused on the BRI2 peptide, which is derived from the amino acid sequence of BRI2 and inhibits the beta pathway of APP processing. We identified peroxiredoxin 1 (PRDX1), an anti-oxidative stress enzyme, as a target protein of this peptide. We also found PRDX1 is functionally required for the inhibition of APP processing by BRI2, hinting a possible link between oxidative stress and APP processing.

Academic Significance and Societal Importance of the Research Achievements

アルツハイマー病(AD)の研究の焦点は、患者脳内に蓄積したベータアミロイドが毒性を呈するというアミロイド仮説に基づいているものが大部分です。しかし、アミロイドを患者脳内から除去しても病状が改善しないなど、アミロイド仮説では、理解も治療も成功しておりません。
本研究は、ADの進行を抑えるBRI2に注目し、他の研究とは別方面からADの病態を解明しようとするものです。BRI2に基づくペプチドを用いて、抗酸化作用を持つ標的蛋白質を同定し、抗酸化作用とAPPの代謝の関連を見つけています。老化のシグナルである酸化的ストレスに対抗する酵素とAPPの代謝の関連は、新しい治療の基礎になりえます。

Report

(4 results)
  • 2018 Annual Research Report   Final Research Report ( PDF )
  • 2017 Research-status Report
  • 2016 Research-status Report
  • Research Products

    (6 results)

All 2019 2018 2017 2016

All Journal Article (1 results) (of which Peer Reviewed: 1 results) Presentation (5 results) (of which Invited: 1 results)

  • [Journal Article] BRI2 as an anti-Alzheimer gene2018

    • Author(s)
      Matsuda Shuji, Senda Takao
    • Journal Title

      Medical Molecular Morphology

      Volume: 印刷中 Issue: 1 Pages: 1-7

    • DOI

      10.1007/s00795-018-0191-1

    • Related Report
      2018 Annual Research Report 2017 Research-status Report
    • Peer Reviewed
  • [Presentation] アルツハイマー病抵抗遺伝子BRI2に関連するPRDX1の作用2019

    • Author(s)
      松田修二、山田名美、千田隆夫
    • Organizer
      第124回日本解剖学会総会・全国学術集会
    • Related Report
      2018 Annual Research Report
  • [Presentation] 抗アルツハイマー遺伝子BRI2に由来するペプチドの性状解析2017

    • Author(s)
      松田修二、山田名美、千田隆夫
    • Organizer
      第122回日本解剖学会総会・全国学術集会
    • Place of Presentation
      長崎県長崎市長崎大学
    • Year and Date
      2017-03-28
    • Related Report
      2016 Research-status Report
  • [Presentation] 抗アルツハイマー遺伝子としてのBRI22017

    • Author(s)
      松田修二、山田名美、千田隆夫
    • Organizer
      第49回日本臨床分子形態学会総会・学術集会
    • Related Report
      2017 Research-status Report
    • Invited
  • [Presentation] アルツハイマー病抵抗遺伝子BRI2に由来するペプチドの性状解析2016

    • Author(s)
      松田修二、山田名美、千田隆夫
    • Organizer
      第76回日本解剖学会中部支部学術集会
    • Place of Presentation
      長野県松本市信州大学
    • Year and Date
      2016-10-09
    • Related Report
      2016 Research-status Report
  • [Presentation] アルツハイマー病抵抗遺伝子BRI2に由来するペプチドの性状解析2016

    • Author(s)
      松田修二、山田名美、千田隆夫
    • Organizer
      第48回日本臨床分子形態学会総会・学術集会
    • Place of Presentation
      熊本県熊本市熊本大学
    • Year and Date
      2016-09-24
    • Related Report
      2016 Research-status Report

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Published: 2016-04-21   Modified: 2020-03-30  

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