MITOCHONDRIA, OXIDATIVE STRESS AND NEURONAL APOPTOSIS: BIOCHEMICAL, CELLULAR AND PHARMACOLOGICAL APPROACHES

线粒体、氧化应激和神经元凋亡:生物化学、细胞和药理学方法

基本信息

  • 批准号:
    nhmrc : 194323
  • 负责人:
  • 金额:
    $ 9.73万
  • 依托单位:
  • 依托单位国家:
    澳大利亚
  • 项目类别:
    NHMRC Project Grants
  • 财政年份:
    2002
  • 资助国家:
    澳大利亚
  • 起止时间:
    2002-01-01 至 2002-12-31
  • 项目状态:
    已结题

项目摘要

Our goal is to understand the detailed process whereby nerve cells die after various stresses and injury. We aim also to develop novel ways of protecting cells against such death. The death of nerve cells plays an important role in a series of neurodegenerative diseases, such as Parkinson's, Huntington's and Motor Neurone Diseases. One prevalent cause of cell death arises from the action of transmitters that normally signal between nerve cells but which, under conditions of stress and injury, cause overstimulation of the nerve cells leading to death (excitotoxicity). Mitochondria are component of cells normally providing energy for the cell to carry out its various functions; but under stress conditions mitochondria act as controllers in cellular decision-making processes leading to cell death. Moreover, mitochondria are known to play an important role in neurodegenerative diseases, as they are a source of damaging oxygen derivatives called free radicals that cause cell injury. Mitochondria are also involved in death resulting from excitotoxicity. In order to understand the detailed mechanism of the nerve cell death process, we will use cultured nerve cells from the brains of laboratory mice, including both normal mice and those that are models of neurodegenerative disease. Injury leading to death will be induced by analogues of the transmitters that cause excitotoxicity. We will concentrate the those aspects of the death process that involve mitochondria, as this will enable us to test a range of antioxidants that can be expected to lead to new drug treatments for neuronal cell injury. Included in these compounds are novel antioxidants that are targeted to mitochondria. This project brings together the expertise in neuroscience and pharmacology of Professor Beart with the skills in biochemistry of Professor Nagley, particularly in mitochondrial and cell death research, to address this important medical research problem in a multidisciplinary manner.
我们的目标是了解神经细胞在各种压力和损伤后死亡的详细过程。我们的目标也是开发保护细胞免受这种死亡的新方法。神经细胞的死亡在帕金森病、亨廷顿病和运动神经元病等一系列神经退行性疾病中起着重要作用。细胞死亡的一个普遍原因是神经递质的作用,这些递质通常在神经细胞之间发出信号,但在应激和损伤的条件下,会导致神经细胞的过度刺激而导致死亡(兴奋性毒性)。线粒体是细胞的组成部分,通常为细胞提供能量以执行其各种功能;但在应激条件下,线粒体在细胞决策过程中充当控制器,导致细胞死亡。此外,已知线粒体在神经退行性疾病中发挥重要作用,因为它们是导致细胞损伤的称为自由基的破坏性氧衍生物的来源。线粒体也参与兴奋性毒性导致的死亡。为了了解神经细胞死亡过程的详细机制,我们将使用来自实验室小鼠大脑的培养神经细胞,包括正常小鼠和神经退行性疾病模型。引起兴奋性毒性的递质的类似物将诱导导致死亡的损伤。我们将集中在涉及线粒体的死亡过程的那些方面,因为这将使我们能够测试一系列抗氧化剂,这些抗氧化剂有望导致神经元细胞损伤的新药物治疗。这些化合物中包括靶向线粒体的新型抗氧化剂。该项目汇集了Beart教授在神经科学和药理学方面的专业知识,以及Nagley教授在生物化学方面的技能,特别是在线粒体和细胞死亡研究方面,以多学科的方式解决这一重要的医学研究问题。

项目成果

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Dr Nam Cheung的其他文献

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