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Pathophysiology and prevention of neuronal damage in major cerebral arterial occlusive disease

Research Project

Project/Area Number 17590910
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Neurology
Research InstitutionKyoto University (2006)
Research Institute, Shiga Medical Center (2005)

Principal Investigator

YAMAUCHI Hiroshi  Kyoto University, Graduate school of medicine, Associate professor, 医学研究科, 助教授 (40360812)

Project Period (FY) 2005 – 2006
Project Status Completed (Fiscal Year 2006)
Budget Amount *help
¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 2006: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2005: ¥2,200,000 (Direct Cost: ¥2,200,000)
Keywordslarge artery disease / selective neuronal damage / benzodiazepine receptor / positron emission tomography / cerebral ischemia / cerebral infarction / benzodiazepine受容体
Research Abstract

In patients with atherothrombotic internal carotid artery (ICA) or middle cerebral artery (MCA) occlusive disease, the chronic reduction in cerebral perfusion pressure (chronic hemodynamic compromise) increases the risk for ischemic neuronal damage. However, the relationship between hemodynamic cerebral ischemia and neuronal damage has not been demonstrated in vivo in humans. The clarification of this relationship is important because vascular reconstruction surgery can improve chronic hemodynamic compromise, which might prevent the development of selective neuronal damage as well as infarction. I investigated the pathophysiology of ischemic neuronal damage in atherothrombotic ICA or MCA occlusive disease by imaging of the central type benzodiazepine receptors (BZR), which are expressed by most cortical neurons, with positrom emission tomography and ^<11>C-Flumazenil. At first, in a cross sectional study, we demonstrated that hemodynamic cerebral ischemia due to atherothrombotic major … More cerebral arterial disease cause selective neuronal damage, by showing that 1) selective neuronal damage demonstrated as decreased BZR is associated with borderzone infarction (hemodynamically induced infarction), and 2)increased oxygen extraction fraction (severe hemodynamic impairment). Then, in a longitudinal study, we confirmed the causal relationship between hemodynamic ischemia and selective neuronal damage by showing that a decrease of BZR during follow-up is associated with an increase of oxygen extraction fraction (hemodynamic deterioration). In patients with atherothrombotic ICA or MCA occlusive disease, selective neuronal damage demonstrated as decreased BZR is associated with chronic hemodynamic compromise (misery perfusion). Misery perfusion may be important for the development of selective neuronal damage in atherothrombotic ICA or MCA occlusive disease. Vascular reconstruction surgery in patients with misery perfusion may lead to the prevention of selective neuronal damage. Imaging of BZR may become a tool for quantitatively evaluating the success of future therapeutic interventions for protecting neurons from ischemic damage. Less

Report

(3 results)
  • 2006 Annual Research Report   Final Research Report Summary
  • 2005 Annual Research Report
  • Research Products

    (9 results)

All 2007 2006 2005

All Journal Article (9 results)

  • [Journal Article] Selective neuronal damage and chronic hemodynamic cerebral ischemia2007

    • Author(s)
      Yamauchi H et al.
    • Journal Title

      Ann Neurol 61・5

      Pages: 454-465

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2006 Final Research Report Summary
  • [Journal Article] Selective neuronal damage and chronic hemodynamic cerebral ischemia2007

    • Author(s)
      Yamauchi H et al.
    • Journal Title

      Ann Neurol 61(in press)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2006 Final Research Report Summary
  • [Journal Article] Selective neuronal damage and chronic hemodynamic cerebral ischemia2007

    • Author(s)
      Yamauchi H. et al.
    • Journal Title

      Ann Neurol 61(in press)

    • Related Report
      2006 Annual Research Report
  • [Journal Article] Focal glucose hypermetabolism in interictal state of west syndrome2006

    • Author(s)
      Kumada T et al.
    • Journal Title

      Pediatr Neurol 34・1

      Pages: 47-50

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2006 Final Research Report Summary
  • [Journal Article] Focal glucose hypermetabolism in interictal state of west syndrome2006

    • Author(s)
      Kumada T et al.
    • Journal Title

      Pediatr Neurol 34

      Pages: 47-50

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2006 Final Research Report Summary
  • [Journal Article] Focal glucose hypermetabolism in interictal state of west syndrome2006

    • Author(s)
      Kumada T, Okazawa H, Yamauchi H, Kitoh T, Ito M
    • Journal Title

      Pediatr Neurol 34・1

      Pages: 47-50

    • Related Report
      2005 Annual Research Report
  • [Journal Article] Selective neuronal damage and borderzone infarction in carotid artery occlusive disease2005

    • Author(s)
      Yamauchi H et al.
    • Journal Title

      J Nucl Med 46・12

      Pages: 1973-1979

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2006 Final Research Report Summary
  • [Journal Article] Selective neuronal damage and borderzone infarction in carotid artery occlusive disease2005

    • Author(s)
      Yamauchi H et al.
    • Journal Title

      J Nucl Med 46

      Pages: 1973-1979

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2006 Final Research Report Summary
  • [Journal Article] Selective neuronal damage and borderzone infarction in carotid artery occlusive disease2005

    • Author(s)
      Yamauchi H, Kudoh T, Kishibe Y, Iwasaki J, Kagawa S
    • Journal Title

      J Nucl Med 46・12

      Pages: 1973-1979

    • Related Report
      2005 Annual Research Report

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Published: 2005-04-01   Modified: 2016-04-21  

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