Laboratory of Proteomics, Institute of Biology, Eötvös Loránd University, Pázmány P. stny 1/C, H-1117 Budapest, Hungary.
Neurochem Int. 2011 Jun;58(7):739-50. doi: 10.1016/j.neuint.2011.02.008. Epub 2011 Feb 17.
Alzheimer's disease (AD) is a protein misfolding-based rapid cognitive impairment in the aging brain. Because of its very widespread molecular background, AD has been approached using genomic and proteomic methods and has accumulated a large body of data during the last 15 years. In this review, we summarize the systems biology data on AD and pay particular attention to the proteomic changes in AD. Applying a systems biology model of the synapse, we attempt to integrate protein changes and provide an explanation of why seemingly diverse molecular changes result in memory impairment. We also summarize the present state of cerebrospinal fluid (CSF) and blood biomarker studies for the diagnosis of AD as well as the results of proteomic studies in tissue cultures and animal models. Finally, we give a systems biology model of AD explaining how AD can develop in an individual manner in each particular subject but always results in a rapidly developing dementia and memory impairment.
阿尔茨海默病（AD）是一种在衰老大脑中以蛋白质错误折叠为基础的快速认知障碍。由于其非常广泛的分子背景，AD 已经通过基因组和蛋白质组学方法进行了研究，并在过去 15 年中积累了大量数据。在这篇综述中，我们总结了 AD 的系统生物学数据，并特别关注 AD 中的蛋白质组变化。我们应用突触的系统生物学模型，尝试整合蛋白质变化，并提供一种解释，说明为什么看似不同的分子变化会导致记忆障碍。我们还总结了目前用于 AD 诊断的脑脊液（CSF）和血液生物标志物研究以及组织培养和动物模型中的蛋白质组学研究的结果。最后，我们给出了一个 AD 的系统生物学模型，解释了 AD 如何在每个特定个体中以个体方式发展，但总是导致快速发展的痴呆和记忆障碍。
