Department of Neurology, Georgetown University Medical Center, Washington, DC, USA; Department of Neuroscience, Georgetown University Medical Center, Washington, DC, USA.
Department of Neurology, University of Rochester School of Medicine, Rochester, NY, USA.
Alzheimers Dement. 2014 Jun;10(3 Suppl):S196-212. doi: 10.1016/j.jalz.2014.04.015.
The increasing number of afflicted individuals with late-onset Alzheimer's disease (AD) poses significant emotional and financial burden on the world's population. Therapeutics designed to treat symptoms or alter the disease course have failed to make an impact, despite substantial investments by governments, pharmaceutical industry, and private donors. These failures in treatment efficacy have led many to believe that symptomatic disease, including both mild cognitive impairment (MCI) and AD, may be refractory to therapeutic intervention. The recent focus on biomarkers for defining the preclinical state of MCI/AD is in the hope of defining a therapeutic window in which the neural substrate remains responsive to treatment. The ability of biomarkers to adequately define the at-risk state may ultimately allow novel or repurposed therapeutic agents to finally achieve the disease-modifying status for AD. In this review, we examine current preclinical AD biomarkers and suggest how to generalize their use going forward.
越来越多的晚发性阿尔茨海默病（AD）患者给世界人口带来了巨大的情感和经济负担。尽管政府、制药行业和私人捐助者投入了大量资金，但旨在治疗症状或改变疾病进程的疗法并未产生影响。这些治疗效果的失败导致许多人认为，包括轻度认知障碍（MCI）和 AD 在内的症状性疾病可能对治疗干预具有抗性。最近，人们关注用于定义 MCI/AD 临床前状态的生物标志物，希望能确定一个治疗窗口期，在此期间，神经基质仍然对治疗有反应。生物标志物能够充分定义高危状态的能力最终可能使新型或重新定位的治疗药物最终实现 AD 的疾病修饰状态。在这篇综述中，我们检查了当前的临床前 AD 生物标志物，并提出了如何在未来推广其使用的建议。
