Nantz National Alzheimer Center, Stanley H. Appel Department of Neurology, Houston Methodist Neurological Institute, Houston Methodist Research Institute, Weill Cornell Medicine, Houston, Texas; and
Nantz National Alzheimer Center, Stanley H. Appel Department of Neurology, Houston Methodist Neurological Institute, Houston Methodist Research Institute, Weill Cornell Medicine, Houston, Texas; and.
J Nucl Med. 2022 Jun;63(Suppl 1):45S-52S. doi: 10.2967/jnumed.121.263200.
Neuroinflammation plays a major role in the etiopathology of neurodegenerative diseases, including Alzheimer and Parkinson diseases, frontotemporal lobar degeneration, and amyotrophic lateral sclerosis. In vivo monitoring of neuroinflammation using PET is critical to understand this process, and data are accumulating in this regard, thus a review is useful. From PubMed, we retrieved publications using any of the available PET tracers to image neuroinflammation in humans as well as selected articles dealing with experimental animal models or the chemistry of currently used or potential radiotracers. We reviewed 280 articles. The most common PET neuroinflammation target, translocator protein (TSPO), has limitations, lacking cellular specificity and the ability to separate neuroprotective from neurotoxic inflammation. However, TSPO PET is useful to define the amount and location of inflammation in the brain of people with neurodegenerative disorders. We describe the characteristics of TSPO and other potential PET neuroinflammation targets and PET tracers available or in development. Despite target and tracer limitations, in recent years there has been a sharp increase in the number of reports of neuroinflammation PET in humans. The most studied has been Alzheimer disease, in which neuroinflammation seems initially neuroprotective and neurotoxic later in the progression of the disease. We describe the findings in all the major neurodegenerative disorders. Neuroinflammation PET is an indispensable tool to understand the process of neurodegeneration, particularly in humans, as well as to validate target engagement in therapeutic clinical trials.
神经炎症在神经退行性疾病（包括阿尔茨海默病和帕金森病、额颞叶痴呆和肌萎缩侧索硬化症）的发病机制中起主要作用。使用正电子发射断层扫描（PET）对神经炎症进行体内监测对于理解这一过程至关重要，并且这方面的数据正在不断积累，因此进行综述很有必要。我们从 PubMed 检索了使用任何可用的 PET 示踪剂来对人类神经炎症进行成像的出版物，以及涉及实验动物模型或当前使用或潜在放射性示踪剂化学的选定文章。我们综述了 280 篇文章。最常见的 PET 神经炎症靶点，即转位蛋白（TSPO），存在局限性，缺乏细胞特异性，无法区分神经保护性炎症和神经毒性炎症。然而，TSPO PET 可用于定义神经退行性疾病患者大脑中炎症的数量和位置。我们描述了 TSPO 及其他潜在 PET 神经炎症靶点和示踪剂的特性，包括已有的和正在开发中的。尽管存在靶点和示踪剂的局限性，但近年来，人类神经炎症 PET 的报道数量急剧增加。研究最多的是阿尔茨海默病，其中神经炎症在疾病进展的早期似乎具有神经保护作用，而后期则具有神经毒性作用。我们描述了所有主要神经退行性疾病中的发现。神经炎症 PET 是理解神经退行性过程的不可或缺的工具，特别是在人类中，也是验证治疗性临床试验中靶点结合的不可或缺的工具。
