Functional copper deficiency models of Alzheimer's disease

阿尔茨海默病的功能性缺铜模型

• 批准号: nhmrc : 454386
• 负责人: Prof James Camakaris
• 金额: $ 30.32万
• 依托单位: The University of Melbourne
• 依托单位国家: 澳大利亚
• 项目类别: NHMRC Project Grants
• 财政年份: 2007
• 资助国家: 澳大利亚
• 起止时间: 2007-01-01 至 2009-12-31
• 项目状态: 已结题
• 来源: https://researchdata.edu.au/functional-copper-deficiency-alzheimers-disease/100841
• 关键词: Functional; copper; deficiency; models; Alzheimer

Alzheimer's disease is a serious neurodegenerative disease which increases in incidence with age. It affects the quality of life and care required for approximately 160,000 Australians and costs the national economy 6.6 billion dollars per annum. Current therapy is of limited efficacy. Our studies are directed towards testing the hypothesis that a functional deficiency of the essential trace element, copper, occurs in the brain with ageing, and this leads to oxidative stress and death of neurons associated with Alzheimer's disease. We will use animal and cell culture models to test this hypothesis which is based on promising preliminary data from such models. We believe that beta amyloid, which accumulates in Alzheimer's brains and is believed to be a major part of the pathological mechanism, has a normal role in maintaining copper balance and that this balance is disturbed by ageing or particular mutations. This research should lead to better treatments using drugs which mobilise copper entry into cells.

阿尔茨海默病是一种严重的神经退行性疾病，其发病率随着年龄的增长而增加。它影响了大约16万澳大利亚人的生活质量和所需的护理，每年给国民经济造成66亿澳元的损失。目前的治疗效果有限。我们的研究是针对测试的假设，即功能性缺乏的基本微量元素，铜，发生在大脑中的老化，这导致氧化应激和死亡的神经元与阿尔茨海默氏病。我们将使用动物和细胞培养模型来测试这一假设，这是基于有希望的初步数据，从这些模型。我们认为，β淀粉样蛋白，它积累在阿尔茨海默氏症的大脑中，被认为是病理机制的主要组成部分，在维持铜平衡方面具有正常作用，这种平衡会受到衰老或特定突变的干扰。这项研究应该会带来更好的治疗方法，使用药物动员铜进入细胞。