A panel of radiochemicals has enabled in vivo positron emission tomography (PET) of tau pathologies in Alzheimer’s disease (AD), although sensitive detection of frontotemporal lobar degeneration (FTLD) tau inclusions has been unsuccessful. Here, we generated an imaging probe, PM-PBB3, for capturing diverse tau deposits. In vitro assays demonstrated the reactivity of this compound with tau pathologies in AD and FTLD. We could also utilize PM-PBB3 for optical/PET imaging of a living murine tauopathy model. A subsequent clinical PET study revealed increased binding of ¹⁸F-PM-PBB3 in diseased patients, reflecting cortical-dominant AD and subcortical-dominant progressive supranuclear palsy (PSP) tau topologies. Notably, the in vivo reactivity of ¹⁸F-PM-PBB3 with FTLD tau inclusion was strongly supported by neuropathological examinations of brains derived from Pick’s disease, PSP, and corticobasal degeneration patients who underwent PET scans. Finally, visual inspection of ¹⁸F-PM-PBB3-PET images was indicated to facilitate individually based identification of diverse clinical phenotypes of FTLD on a neuropathological basis.

尽管对额颞叶变性（FTLD）tau夹杂物的灵敏检测尚未成功，但一组放射化学物质已使tau病理的体内正电子发射断层扫描（PET）成为可能。在这里，我们生成了一个成像探针PM-PBB3，用于捕获各种tau沉积物。体外试验证明了该化合物与AD和FTLD中tau病理的反应性。我们还可以将PM-PBB3用于活体鼠tauopathy模型的光学/ PET成像。随后的一项临床PET研究表明，患病患者中¹⁸ F-PM-PBB3的结合增加，反映出皮质占优势的AD和皮质下占优势的进行性核上性麻痹（PSP）tau拓扑结构。值得注意的是，体内的反应¹⁸架F-PM-PBB3与FTLD头包含强烈由匹克氏病，PSP，和谁接受PET扫描皮质基底节变性患者的脑部神经病理学检验支持。最后，需要目视检查¹⁸ F-PM-PBB3-PET图像，以利于在神经病理学基础上基于个体识别FTLD的各种临床表型。