Abstract
Introduction: The PET radioligand, 18 F-THK5351, was initially developed to target tau aggregation present in neurofibrillary tangles. However, 18 F-THK5351 was recently reported to bind to monoamine oxidase B (MAO-B) with a certain level of affinity. MAO-B is highly concentrated in astrocytes. MAO-B concentration increases during so-called "gliosis", which is a spectrum of changes in astrocytes that occur after brain injury. Wallerian degeneration of the pyramidal tract usually develops after a cerebral infarction including primary motor cortex. In the early stage, axonal swelling and breakdown of myelin sheath occur. In the later stage, the degenerated axons are replaced by gliosis, which is primarily the proliferation of astrocytes to form a scar. These suggest that 18 F-THK5351 concentrates in the lesion where gliosis occurs in the process of Wallerian degeneration. We now present a case showing a potential use of 18 F-THK5351 PET to identify Wallerian degeneration of the pyramidal tract after a cerebral infarction. Methods: A patient developed left-sided hemiplegia caused by a right middle cerebral artery infarction at the age of 39, and underwent 18 F-THK5351 PET at ages 41 and 42. Emission data were acquired for 20 min starting at 40 min after an intravenous injection of 18 F-THK5351. Images were normalized using the cerebellum as a reference region Results: 18 F-THK5351 images at ages 41 and 42 showed intense uptake along the ipsilateral pyramidal tract from the corona radiata to the medulla (Figure 1, arrows). 18 F-THK5351 uptake slightly decreased at the age of 42. Conclusion: 18 F-THK5351 PET can identify Wallerian degeneration of the pyramidal tract accompanied with gliosis by targeting MAO-B located. This case suggests that gliosis in the process of Wallerian degeneration of the pyramidal tract still remains even three years after the stroke. Figure1: MRI (A) and 18 F-THK5351 images superimposed on MRI at ages 41 (B) and 42 (C)
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