Cavedo E, Lista S, Khachaturian Z, Aisen P, Amouyel P, Herholz K, Jack C R, Sperling R, Cummings J, Blennow K, O'Bryant S, Frisoni G B, Khachaturian A, Kivipelto M, Klunk W, Broich K, Andrieu S, de Schotten M Thiebaut, Mangin J-F, Lammertsma A A, Johnson K, Teipel S, Drzezga A, Bokde A, Colliot O, Bakardjian H, Zetterberg H, Dubois B, Vellas B, Schneider L S, Hampel H
Sorbonne Universités, Université Pierre et Marie Curie, Paris 06, Institut de la Mémoire et de la Maladie d'Alzheimer (IM2A) Hôpital de la Pitié-Salpétrière & Institut du Cerveau et de la Moelle épinière (ICM), UMR S 1127, Hôpital de la Pitié-Salpétrière Paris & CATI multicenter neuroimaging platform, France; Laboratory of Epidemiology, Neuroimaging and Telemedicine, IRCCS San Giovanni di Dio Fatebenefratelli Brescia, Italy.
AXA Research Fund & UPMC Chair; Sorbonne Universités, Université Pierre et Marie Curie, Paris 06, Institut de la Mémoire et de la Maladie d'Alzheimer (IM2A) Hôpital de la Pitié-Salpétrière & Inserm U1127 Institut du Cerveau et de la Moelle épinière (ICM), Hôpital de la Pitié-Salpétrière Paris, France.
J Prev Alzheimers Dis. 2014 Dec;1(3):181-202. doi: 10.14283/jpad.2014.32.
Alzheimer's disease (AD) is a slowly progressing non-linear dynamic brain disease in which pathophysiological abnormalities, detectable in vivo by biological markers, precede overt clinical symptoms by many years to decades. Use of these biomarkers for the detection of early and preclinical AD has become of central importance following publication of two international expert working group's revised criteria for the diagnosis of AD dementia, mild cognitive impairment (MCI) due to AD, prodromal AD and preclinical AD. As a consequence of matured research evidence six AD biomarkers are sufficiently validated and partly qualified to be incorporated into operationalized clinical diagnostic criteria and use in primary and secondary prevention trials. These biomarkers fall into two molecular categories: biomarkers of amyloid-beta (Aβ) deposition and plaque formation as well as of tau-protein related hyperphosphorylation and neurodegeneration. Three of the six gold-standard ("core feasible) biomarkers are neuroimaging measures and three are cerebrospinal fluid (CSF) analytes. CSF Aβ1-42 (Aβ1-42), also expressed as Aβ1-42 : Aβ1-40 ratio, T-tau, and P-tau Thr181 & Thr231 proteins have proven diagnostic accuracy and risk enhancement in prodromal MCI and AD dementia. Conversely, having all three biomarkers in the normal range rules out AD. Intermediate conditions require further patient follow-up. Magnetic resonance imaging (MRI) at increasing field strength and resolution allows detecting the evolution of distinct types of structural and functional abnormality pattern throughout early to late AD stages. Anatomical or volumetric MRI is the most widely used technique and provides local and global measures of atrophy. The revised diagnostic criteria for "prodromal AD" and "mild cognitive impairment due to AD" include hippocampal atrophy (as the fourth validated biomarker), which is considered an indicator of regional neuronal injury. Advanced image analysis techniques generate automatic and reproducible measures both in regions of interest, such as the hippocampus and in an exploratory fashion, observer and hypothesis-indedendent, throughout the entire brain. Evolving modalities such as diffusion-tensor imaging (DTI) and advanced tractography as well as resting-state functional MRI provide useful additionally useful measures indicating the degree of fiber tract and neural network disintegration (structural, effective and functional connectivity) that may substantially contribute to early detection and the mapping of progression. These modalities require further standardization and validation. The use of molecular in vivo amyloid imaging agents (the fifth validated biomarker), such as the Pittsburgh Compound-B and markers of neurodegeneration, such as fluoro-2-deoxy-D-glucose (FDG) (as the sixth validated biomarker) support the detection of early AD pathological processes and associated neurodegeneration. How to use, interpret, and disclose biomarker results drives the need for optimized standardization. Multimodal AD biomarkers do not evolve in an identical manner but rather in a sequential but temporally overlapping fashion. Models of the temporal evolution of AD biomarkers can take the form of plots of biomarker severity (degree of abnormality) versus time. AD biomarkers can be combined to increase accuracy or risk. A list of genetic risk factors is increasingly included in secondary prevention trials to stratify and select individuals at genetic risk of AD. Although most of these biomarker candidates are not yet qualified and approved by regulatory authorities for their intended use in drug trials, they are nonetheless applied in ongoing clinical studies for the following functions: (i) inclusion/exclusion criteria, (ii) patient stratification, (iii) evaluation of treatment effect, (iv) drug target engagement, and (v) safety. Moreover, novel promising hypothesis-driven, as well as exploratory biochemical, genetic, electrophysiological, and neuroimaging markers for use in clinical trials are being developed. The current state-of-the-art and future perspectives on both biological and neuroimaging derived biomarker discovery and development as well as the intended application in prevention trials is outlined in the present publication.
阿尔茨海默病(AD)是一种进展缓慢的非线性动态脑部疾病,其病理生理异常可通过生物标志物在体内检测到,比明显的临床症状早出现数年至数十年。在两个国际专家工作组发布了AD痴呆、AD所致轻度认知障碍(MCI)、前驱AD和临床前期AD的修订诊断标准后,使用这些生物标志物来检测早期和临床前期AD变得至关重要。由于研究证据的成熟,六种AD生物标志物已得到充分验证,部分符合纳入可实施的临床诊断标准并用于一级和二级预防试验的条件。这些生物标志物分为两类分子:淀粉样β蛋白(Aβ)沉积和斑块形成的生物标志物,以及tau蛋白相关的过度磷酸化和神经变性的生物标志物。六种金标准(“核心可行”)生物标志物中有三种是神经影像学测量指标,三种是脑脊液(CSF)分析物。脑脊液Aβ1-42(Aβ1-42),也表示为Aβ1-42:Aβ1-40比值、总tau蛋白(T-tau)以及磷酸化tau蛋白Thr181和Thr231已被证明在MCI前驱期和AD痴呆中具有诊断准确性和风险增强作用。相反,所有三种生物标志物都在正常范围内则可排除AD。处于中间状态的情况需要对患者进行进一步随访。随着场强和分辨率的提高,磁共振成像(MRI)能够检测到从AD早期到晚期不同类型的结构和功能异常模式的演变。解剖学或体积MRI是使用最广泛的技术,可提供局部和整体的萎缩测量。“前驱AD ”和“AD所致轻度认知障碍”的修订诊断标准包括海马萎缩(作为第四种已验证的生物标志物),其被认为是区域神经元损伤的指标。先进的图像分析技术能够在感兴趣区域(如海马)自动生成可重复的测量结果,并以探索性方式在整个大脑中进行观察者和假设独立的测量。诸如扩散张量成像(DTI)和先进的纤维束成像以及静息态功能MRI等不断发展的成像方式提供了额外有用的测量结果,表明纤维束和神经网络解体的程度(结构、有效和功能连接性),这可能对早期检测和疾病进展的映射有很大帮助。这些成像方式需要进一步标准化和验证。使用分子体内淀粉样蛋白成像剂(第五种已验证的生物标志物),如匹兹堡化合物B,以及神经变性标志物,如氟代脱氧葡萄糖(FDG)(作为第六种已验证的生物标志物),有助于检测早期AD病理过程及相关神经变性。如何使用、解释和披露生物标志物结果推动了对优化标准化的需求。多模态AD生物标志物并非以相同方式演变,而是以连续但时间上重叠的方式演变。AD生物标志物的时间演变模型可以采用生物标志物严重程度(异常程度)与时间的关系图形式。AD生物标志物可以组合使用以提高准确性或风险。越来越多的遗传风险因素列表被纳入二级预防试验,以对有AD遗传风险的个体进行分层和选择。尽管这些生物标志物候选物中的大多数尚未得到监管机构的合格认定和批准用于药物试验,但它们仍被应用于正在进行的临床研究中以实现以下功能:(i)纳入/排除标准,(ii)患者分层,(iii)治疗效果评估,(iv)药物靶点参与度,以及(v)安全性。此外,正在开发用于临床试验的新型有前景的基于假设驱动的以及探索性的生化、遗传、电生理和神经影像学标志物。本出版物概述了生物和神经影像学衍生生物标志物发现与开发的当前技术水平和未来前景,以及在预防试验中的预期应用。