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Role of Nrf1 activation in progressive neurodegeneration

Research Project

Project/Area Number 24590370
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Pathological medical chemistry
Research InstitutionTohoku University

Principal Investigator

NISHIJIMA Ichiko  東北大学, 東北メディカル・メガバンク機構, 講師 (70600394)

Co-Investigator(Renkei-kenkyūsha) KATSUOKA Fumiki  東北大学, 東北メディカル・メガバンク機構, 准教授 (30447255)
AOKI Masashi  東北大学, 大学院医学系研究科, 教授 (70302148)
Project Period (FY) 2012-04-01 – 2016-03-31
Project Status Completed (Fiscal Year 2015)
Budget Amount *help
¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Keywords脳神経疾患 / 発現制御 / モデル動物 / H46R変異SOD1遺伝子発現マウス / Nrf1遺伝子発現マウス / Nrf1遺伝子欠損マウス / 神経変性 / Nrf1 / プロテアソーム / 筋萎縮性側索硬化症 / モデルマウス / hSOD1
Outline of Final Research Achievements

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease of motor neurons. Although defective ubiquitin-proteasome system is associated with neurodegenerative diseases commonly, the underlying molecular mechanisms are still unknown. To understand defense mechanisms using ubiquitin-proteasome system against progressive degeneration of neurons, we have analyzed Nrf1 activation in neurodegenerative disease condition using the compound transgenic mice carrying Nrf1 and mutant human SOD1 genes. The compound transgenic mice overexpressed Nrf1 and mutant human SOD1 have similar onset of neurodegeneration to mutant SOD1 transgenic mice. However, their degenerative progression was faster than mutant SOD1 transgenic mice. Our data indicate that Nrf1 activation may contribute acceleration of neurodegenerative disorders.

Report

(5 results)
  • 2015 Annual Research Report   Final Research Report ( PDF )
  • 2014 Research-status Report
  • 2013 Research-status Report
  • 2012 Research-status Report
  • Research Products

    (4 results)

All 2015 2012

All Journal Article (3 results) (of which Peer Reviewed: 2 results,  Open Access: 2 results,  Acknowledgement Compliant: 1 results) Presentation (1 results)

  • [Journal Article] Secretin Receptor Involvement in Prion-Infected Cells and Animals2015

    • Author(s)
      Kimura T, Nishizawa K, Oguma A., Nishimura Y, Sakasegawa Y, Teruya K, Nishijima I, Doh-ura K.
    • Journal Title

      FEBS Letters

      Volume: 589 Issue: 15 Pages: 2011-2018

    • DOI

      10.1016/j.febslet.2015.05.039

    • Related Report
      2015 Annual Research Report
    • Peer Reviewed / Open Access
  • [Journal Article] Activation of supraoptic oxytocin neurons by secretin facilitates social recognition.2015

    • Author(s)
      Takayanagi Y, Yoshida M, Takashima A, Takanami K, Yoshida S, Nishimori K, Nishijima I, Sakamoto H, Yamagata T, Onaka T
    • Journal Title

      Biological Psychiatry

      Volume: in press Issue: 3 Pages: 243-251

    • DOI

      10.1016/j.biopsych.2015.11.021

    • Related Report
      2015 Annual Research Report
    • Peer Reviewed / Open Access / Acknowledgement Compliant
  • [Journal Article] 脳の発達における神経ペプチドセクレチンの役割2012

    • Author(s)
      西島維知子
    • Journal Title

      日本生物学的精神医学会誌

      Volume: 23 Pages: 287-291

    • NAID

      130005395431

    • Related Report
      2012 Research-status Report
  • [Presentation] The effects of secretin in postnatal cerebellar development2015

    • Author(s)
      西島 維知子, Bahram Khosravi, 峯岸 直子
    • Organizer
      第38回日本神経科学大会
    • Place of Presentation
      神戸国際会議場、神戸国際展示場(兵庫県 神戸市)
    • Year and Date
      2015-07-28
    • Related Report
      2015 Annual Research Report

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Published: 2013-05-31   Modified: 2019-07-29  

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