Genetic mechanisms that moderate effects of Aβ accumulation in preclinical Alzheimer's disease

阿尔茨海默病(AD)是最常见的痴呆症形式，到2050年，患有该病的人数将增加两倍。目前还没有治愈阿尔茨海默病的方法，减缓不断增长的流行病的唯一手段就是推迟发病。我们建议了解阿尔茨海默病的遗传、认知、神经成像和生物标志物之间的复杂相互作用，以便更好地了解疾病过程，进而识别临床试验的高危个体，并发现疾病修改策略。

Alzheimer’s disease (AD) is the most common form of dementia, and the number of people living with it will triple by 2050. There is currently no cure for AD, and the only means of slow the growing epidemic is to delay onset. We propose to understand the complex interplay between genetic, cognitive, neuroimaging and biological markers of AD in order to better understand the disease process, and in turn identify high-risk individuals for clinical trials and uncover disease-modifying strategies.