GE Healthcare, Amersham, UK.
Centre for Medical Image Computing (CMIC), Department of Medical Physics and Bioengineering, University College London, London, UK.
Eur J Nucl Med Mol Imaging. 2022 Aug;49(10):3508-3528. doi: 10.1007/s00259-022-05784-y. Epub 2022 Apr 7.
Amyloid-β (Aβ) pathology is one of the earliest detectable brain changes in Alzheimer's disease (AD) pathogenesis. The overall load and spatial distribution of brain Aβ can be determined in vivo using positron emission tomography (PET), for which three fluorine-18 labelled radiotracers have been approved for clinical use. In clinical practice, trained readers will categorise scans as either Aβ positive or negative, based on visual inspection. Diagnostic decisions are often based on these reads and patient selection for clinical trials is increasingly guided by amyloid status. However, tracer deposition in the grey matter as a function of amyloid load is an inherently continuous process, which is not sufficiently appreciated through binary cut-offs alone. State-of-the-art methods for amyloid PET quantification can generate tracer-independent measures of Aβ burden. Recent research has shown the ability of these quantitative measures to highlight pathological changes at the earliest stages of the AD continuum and generate more sensitive thresholds, as well as improving diagnostic confidence around established binary cut-offs. With the recent FDA approval of aducanumab and more candidate drugs on the horizon, early identification of amyloid burden using quantitative measures is critical for enrolling appropriate subjects to help establish the optimal window for therapeutic intervention and secondary prevention. In addition, quantitative amyloid measurements are used for treatment response monitoring in clinical trials. In clinical settings, large multi-centre studies have shown that amyloid PET results change both diagnosis and patient management and that quantification can accurately predict rates of cognitive decline. Whether these changes in management reflect an improvement in clinical outcomes is yet to be determined and further validation work is required to establish the utility of quantification for supporting treatment endpoint decisions. In this state-of-the-art review, several tools and measures available for amyloid PET quantification are summarised and discussed. Use of these methods is growing both clinically and in the research domain. Concurrently, there is a duty of care to the wider dementia community to increase visibility and understanding of these methods.
淀粉样蛋白-β(Aβ)病理学是阿尔茨海默病(AD)发病机制中最早可检测到的大脑变化之一。正电子发射断层扫描(PET)可在体内确定大脑 Aβ 的总负荷和空间分布,已有三种氟-18 标记放射性示踪剂获准用于临床使用。在临床实践中,经过培训的读者将根据视觉检查将扫描结果分类为 Aβ 阳性或阴性。诊断决策通常基于这些读取结果,并且越来越多地根据淀粉样蛋白状态选择患者参加临床试验。然而,示踪剂在灰质中的沉积与淀粉样蛋白负荷呈函数关系,这是一个连续的过程,仅通过二进制截止值无法充分理解。用于淀粉样蛋白 PET 定量的最先进方法可以生成与示踪剂无关的 Aβ 负担测量值。最近的研究表明,这些定量测量值能够突出 AD 连续体早期阶段的病理变化,并生成更敏感的阈值,同时提高围绕既定二进制截止值的诊断信心。随着最近 FDA 批准 aducanumab 和更多候选药物的出现,使用定量测量值早期识别淀粉样蛋白负担对于招募合适的受试者至关重要,有助于确定治疗干预和二级预防的最佳窗口期。此外,定量淀粉样蛋白测量值用于临床试验中的治疗反应监测。在临床环境中,大型多中心研究表明,淀粉样蛋白 PET 结果改变了诊断和患者管理,并且定量可以准确预测认知能力下降的速度。这些管理上的变化是否反映出临床结局的改善还有待确定,需要进一步的验证工作来确定定量在支持治疗终点决策方面的效用。在这篇最新综述中,总结和讨论了几种可用于淀粉样蛋白 PET 定量的工具和测量方法。这些方法在临床和研究领域的使用都在增加。同时,有责任提高痴呆症社区对这些方法的可见度和理解。