Functional copper deficiency models of Alzheimer's disease

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16万澳大利亚人所需的生活质量和护理，每年给国家经济造成66亿美元的损失。目前的治疗方法疗效有限。我们的研究旨在验证这样一种假设，即随着年龄的增长，大脑中会出现必要的微量元素铜的功能缺陷，这会导致与阿尔茨海默病相关的神经元的氧化应激和死亡。我们将使用动物和细胞培养模型来检验这一假说，这一假说是基于这些模型中有希望的初步数据。我们认为，聚集在阿尔茨海默病患者大脑中的β淀粉样蛋白被认为是阿尔茨海默病发病机制的主要组成部分，它在维持铜平衡方面发挥着正常作用，这种平衡会受到衰老或特定突变的干扰。这项研究应该会导致使用动员铜进入细胞的药物进行更好的治疗。

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.