Longitudinal changes in ¹⁸F‐<scp>THK</scp>5351 positron emission tomography in corticobasal syndrome

Abstract

Background and purpose Corticobasal syndrome ( CBS ) is pathologically characterized by tau deposits in neuronal and glial cells and by reactive astrogliosis. In several neurodegenerative disorders, 18 F‐ THK 5351 has been observed to bind to reactive astrocytes expressing monoamine oxidase B. In this study, the aim was to investigate the progression of disease‐related pathology in the brains of patients with CBS using positron emission tomography with 18 F‐ THK 5351. Methods Baseline and 1‐year follow‐up imaging were acquired using magnetic resonance imaging and positron emission tomography with 18 F‐ THK 5351 in 10 subjects: five patients with CBS and five age‐matched normal controls ( NC s). Results The 1‐year follow‐up scan images revealed that 18 F‐ THK 5351 retention had significantly increased in the superior parietal gyrus of the patients with CBS compared with the NC s. The median increases in 18 F‐ THK 5351 accumulation in the patients with CBS were 6.53% in the superior parietal gyrus, 4.34% in the precentral gyrus and 4.33% in the postcentral gyrus. In contrast, there was no significant increase in the regional 18 F‐ THK 5351 retention in the NC s. Conclusions Longitudinal increases in 18 F‐ THK 5351 binding can be detected over a short interval in the cortical sites of patients with CBS . A monoamine oxidase B binding radiotracer could be useful in monitoring the progression of astrogliosis in CBS .