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Measuremrnt of laminins in cerebrospinal fluid (CSF) obtained from dementia using antibodies against laminin and laminin peptide -Developping a diagnostic biological marker-

Research Project

Project/Area Number 11670953
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Psychiatric science
Research InstitutionMiyazaki Medical College

Principal Investigator

MATSUDA Kazunori  Miyazaki Medical College, Research Associate, 医学部, 助手 (30311880)

Co-Investigator(Kenkyū-buntansha) 林 要人  宮崎医科大学, 医学部, 助手 (20295223)
田代 謙一郎  九州保健福祉大学, 保健科学部, 教授 (00216954)
Project Period (FY) 1999 – 2000
Project Status Completed (Fiscal Year 2000)
Budget Amount *help
¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2000: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1999: ¥800,000 (Direct Cost: ¥800,000)
KeywordsLaminin / Laminin peptide / Alzheimer's disease / Vascular dementia / ELISA / Cerebrospinal fluid / Diagnostic marker / Therapeutic agent / Therapeutic agent / ラミニンγ / wholeラミニン / ラミニンペプチド / 髄液 / アルツハイマー病(AD) / 脳血管性痴呆(VaD) / βアミロイド
Research Abstract

We developed a new ELISA system using antibodies against whole laminin-1, α5 chain, β1 chain, γ1 chain and laminin peptide (YFQRYLI). Using this ELISA system, we measured laminin levels in CSF obtained from Alzheimer type dementia (ATD), vascular dementia (VaD) and other dementia comparing with normal controls. ATD group showed a significantly lower level of γ1 chain, and the γ1 level of early -onset AD was significantly decreased with aging. On the other hand, late onset AD group showed a significantly higher level of laminin peptide (YFQRYLI) than early-onset AD group and normal controls. VaD group showed a significantly higer level of whole laminin-1 and β1 chain. These results suggest that laminin or its derivatives may correlate to pathogenesis of ATD and VaD, and that the preventing of laminin proteolysis may be an effective therapeutic method for preventing or slowing down the progression of ATD.Furthermore, the assay of CSF laminin for the diagnosis of ATD showed efficient diagnostic sensitivity (81%) and specificity (85%) by using the ratio of CSF tau to CSF whole laminin-1. These findings suggest that the assay of CSF laminin may be useful as a diagnostic biological marker of AD and VaD.

Report

(3 results)
  • 2000 Annual Research Report   Final Research Report Summary
  • 1999 Annual Research Report
  • Research Products

    (5 results)

All Other

All Publications (5 results)

  • [Publications] 松田一典: "アルツハイマー型痴呆(ATD)と脳血管性痴呆(VaD)におけるラミニンの関与-生物学的診断マーカーと治療薬を目的として-"精神薬療研究年報. 33. 172-179 (2001)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2000 Final Research Report Summary
  • [Publications] K.Matsuda, K.Tashiro, Y.Hayashi, A.Monji, I.Yoshida and Y.Mitsuyama: "A study of laminin in cerebrospinal fluid (CSF) obtained from Alzheimer's disease (AD) and vascular dementia (VaD) -For developping an effective therapeutic agent and a diagnostic biological marker-"Ann.Rep.Welfide Medicinal Res.Found.. 33. 172-179 (2001)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2000 Final Research Report Summary
  • [Publications] Tashiro K,Monji A,Yoshida I,Hayashi Y,Matsuda K,Tashiro N,Mitsuyama Y: "An IKLLI-containing peptide derived from the laminin α 1 chain mediating heparin-bindeing,cell adhesion,neurite outgrowth and proliferation,represents a binding site for integrin α 3 β 1 and heparan salphate proteoglycan"Biochemical J.. 40. 1119-1126 (1999)

    • Related Report
      1999 Annual Research Report
  • [Publications] 田代謙一郎、門司 晃、林 要人、松田一典、吉田一郎、三山吉夫: "アルツハイマー病の病態解明と治療薬開発を目的とした、ラミニン活性ペプチドの研究"精神薬療基金研究年報. 31. 211-216 (1999)

    • Related Report
      1999 Annual Research Report
  • [Publications] Monji A,Tashiro K,Yoshida I,Kaname H,Hayashi Y,Matsuda K,Tasiro N: "Laminin inhibits both Aβ40 and Aβ42 fibril formation but does not effect Aβ40 or Aβ42-induced cytotoxicity in PC12 cells."Neurosciences Letters. 266. 85-88 (1999)

    • Related Report
      1999 Annual Research Report

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Published: 1999-04-01   Modified: 2016-04-21  

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