Weiner Michael W, Veitch Dallas P, Aisen Paul S, Beckett Laurel A, Cairns Nigel J, Cedarbaum Jesse, Green Robert C, Harvey Danielle, Jack Clifford R, Jagust William, Luthman Johan, Morris John C, Petersen Ronald C, Saykin Andrew J, Shaw Leslie, Shen Li, Schwarz Adam, Toga Arthur W, Trojanowski John Q
Department of Veterans Affairs Medical Center, Center for Imaging of Neurodegenerative Diseases, San Francisco, CA, USA; Department of Radiology, University of California, San Francisco, CA, USA; Department of Medicine, University of California, San Francisco, CA, USA; Department of Psychiatry, University of California, San Francisco, CA, USA; Department of Neurology, University of California, San Francisco, CA, USA.
Department of Veterans Affairs Medical Center, Center for Imaging of Neurodegenerative Diseases, San Francisco, CA, USA.
Alzheimers Dement. 2015 Jun;11(6):e1-120. doi: 10.1016/j.jalz.2014.11.001.
The Alzheimer's Disease Neuroimaging Initiative (ADNI) is an ongoing, longitudinal, multicenter study designed to develop clinical, imaging, genetic, and biochemical biomarkers for the early detection and tracking of Alzheimer's disease (AD). The initial study, ADNI-1, enrolled 400 subjects with early mild cognitive impairment (MCI), 200 with early AD, and 200 cognitively normal elderly controls. ADNI-1 was extended by a 2-year Grand Opportunities grant in 2009 and by a competitive renewal, ADNI-2, which enrolled an additional 550 participants and will run until 2015. This article reviews all papers published since the inception of the initiative and summarizes the results to the end of 2013. The major accomplishments of ADNI have been as follows: (1) the development of standardized methods for clinical tests, magnetic resonance imaging (MRI), positron emission tomography (PET), and cerebrospinal fluid (CSF) biomarkers in a multicenter setting; (2) elucidation of the patterns and rates of change of imaging and CSF biomarker measurements in control subjects, MCI patients, and AD patients. CSF biomarkers are largely consistent with disease trajectories predicted by β-amyloid cascade (Hardy, J Alzheimer's Dis 2006;9(Suppl 3):151-3) and tau-mediated neurodegeneration hypotheses for AD, whereas brain atrophy and hypometabolism levels show predicted patterns but exhibit differing rates of change depending on region and disease severity; (3) the assessment of alternative methods of diagnostic categorization. Currently, the best classifiers select and combine optimum features from multiple modalities, including MRI, [(18)F]-fluorodeoxyglucose-PET, amyloid PET, CSF biomarkers, and clinical tests; (4) the development of blood biomarkers for AD as potentially noninvasive and low-cost alternatives to CSF biomarkers for AD diagnosis and the assessment of α-syn as an additional biomarker; (5) the development of methods for the early detection of AD. CSF biomarkers, β-amyloid 42 and tau, as well as amyloid PET may reflect the earliest steps in AD pathology in mildly symptomatic or even nonsymptomatic subjects and are leading candidates for the detection of AD in its preclinical stages; (6) the improvement of clinical trial efficiency through the identification of subjects most likely to undergo imminent future clinical decline and the use of more sensitive outcome measures to reduce sample sizes. Multimodal methods incorporating APOE status and longitudinal MRI proved most highly predictive of future decline. Refinements of clinical tests used as outcome measures such as clinical dementia rating-sum of boxes further reduced sample sizes; (7) the pioneering of genome-wide association studies that leverage quantitative imaging and biomarker phenotypes, including longitudinal data, to confirm recently identified loci, CR1, CLU, and PICALM and to identify novel AD risk loci; (8) worldwide impact through the establishment of ADNI-like programs in Japan, Australia, Argentina, Taiwan, China, Korea, Europe, and Italy; (9) understanding the biology and pathobiology of normal aging, MCI, and AD through integration of ADNI biomarker and clinical data to stimulate research that will resolve controversies about competing hypotheses on the etiopathogenesis of AD, thereby advancing efforts to find disease-modifying drugs for AD; and (10) the establishment of infrastructure to allow sharing of all raw and processed data without embargo to interested scientific investigators throughout the world.
阿尔茨海默病神经影像学倡议(ADNI)是一项正在进行的纵向多中心研究,旨在开发用于早期检测和跟踪阿尔茨海默病(AD)的临床、影像学、遗传学和生物化学生物标志物。最初的研究ADNI - 1招募了400名早期轻度认知障碍(MCI)患者、200名早期AD患者和200名认知正常的老年对照。2009年,ADNI - 1通过一项为期2年的重大机遇资助以及一项竞争性延续项目ADNI - 2得到扩展,ADNI - 2又招募了550名参与者,并将持续到2015年。本文回顾了该倡议启动以来发表的所有论文,并总结了截至2013年底的结果。ADNI的主要成就如下:(1)在多中心环境中开发了用于临床试验、磁共振成像(MRI)、正电子发射断层扫描(PET)和脑脊液(CSF)生物标志物的标准化方法;(2)阐明了对照受试者、MCI患者和AD患者中影像学和CSF生物标志物测量的变化模式和速率。CSF生物标志物在很大程度上与β - 淀粉样蛋白级联反应(Hardy,J Alzheimer's Dis 2006;9(增刊3):151 - 3)和AD的tau介导的神经退行性变假说预测的疾病轨迹一致,而脑萎缩和代谢减退水平显示出预测模式,但根据区域和疾病严重程度表现出不同的变化速率;(3)评估诊断分类的替代方法。目前,最佳分类器从多种模式中选择并组合最佳特征,包括MRI、[(18)F] - 氟脱氧葡萄糖 - PET、淀粉样蛋白PET、CSF生物标志物和临床试验;(4)开发用于AD的血液生物标志物,作为用于AD诊断的CSF生物标志物的潜在非侵入性和低成本替代物,并评估α - 突触核蛋白作为一种额外的生物标志物;(5)开发AD的早期检测方法。CSF生物标志物β - 淀粉样蛋白42和tau以及淀粉样蛋白PET可能反映轻度症状甚至无症状受试者中AD病理的最早阶段,并且是在临床前期检测AD的主要候选指标;(6)通过识别最有可能在未来即将出现临床衰退的受试者并使用更敏感的结局指标来减少样本量,从而提高临床试验效率。纳入APOE状态和纵向MRI的多模式方法被证明对未来衰退的预测性最高。用作结局指标的临床试验的改进,如临床痴呆评定量表 - 方框总和,进一步减少了样本量;(7)开创全基因组关联研究,利用定量影像学和生物标志物表型,包括纵向数据,来确认最近确定的基因座CR1、CLU和PICALM,并识别新的AD风险基因座;(8)通过在日本、澳大利亚、阿根廷、中国台湾、韩国以及欧洲和意大利建立类似ADNI的项目,在全球范围内产生影响;(9)通过整合ADNI生物标志物和临床数据来理解正常衰老、MCI和AD的生物学和病理生物学,以促进解决关于AD病因发病机制的相互竞争假说的争议的研究,从而推动寻找AD疾病修饰药物的努力;(十)建立基础设施,允许在无禁运的情况下向全世界感兴趣的科学研究人员共享所有原始和处理后的数据。