Akio Kikuchi1, Nobuyuki Okamura1, Takafumi Hasegawa2, Ryuichi Harada2, Shoichi Watanuki2, Yoshihito Funaki2, Kotaro Hiraoka2, Toru Baba2, Naoto Sugeno2, Ryuji Oshima2, Shun Yoshida2, Junpei Kobayashi2, Michinori Ezura2, Michiko Kobayashi2, Ohito Tano2, Shunji Mugikura2, Ren Iwata2, Aiko Ishiki2, Katsutoshi Furukawa2, Hiroyuki Arai2, Shozo Furumoto2, Manabu Tashiro2, Kazuhiko Yanai2, Yukitsuka Kudo2, Atsushi Takeda2, Masashi Aoki2. 1. From the Departments of Neurology (A.K., T.H., T.B., N.S., R.O., S.Y., J.K., M.E., M.A.), Pharmacology (N.O., R.H., K.Y.), and Diagnostic Radiology (S.M.), Tohoku University Graduate School of Medicine; Divisions of Cyclotron Nuclear Medicine (S.W., K.H., M.T.) and Radiopharmaceutical Chemistry (Y.F., R.I., S.F.), Cyclotron and Radioisotope Center, and Department of Geriatric and Respiratory Medicine (A.I., K.F., H.A.) and Division of Neuroimaging (Y.K.), Institute of Development, Aging and Cancer, Tohoku University; Department of Neurology (M.K.), Tohoku Pharmaceutical University Hospital; Department of Neurology (O.T.), Sendai Medical Center; and Department of Neurology (A.T.), National Hospital Organization, Sendai Nishitaga Hospital, Sendai, Japan. akikuchi@med.tohoku.ac.jp nookamura@med.tohoku.ac.jp. 2. From the Departments of Neurology (A.K., T.H., T.B., N.S., R.O., S.Y., J.K., M.E., M.A.), Pharmacology (N.O., R.H., K.Y.), and Diagnostic Radiology (S.M.), Tohoku University Graduate School of Medicine; Divisions of Cyclotron Nuclear Medicine (S.W., K.H., M.T.) and Radiopharmaceutical Chemistry (Y.F., R.I., S.F.), Cyclotron and Radioisotope Center, and Department of Geriatric and Respiratory Medicine (A.I., K.F., H.A.) and Division of Neuroimaging (Y.K.), Institute of Development, Aging and Cancer, Tohoku University; Department of Neurology (M.K.), Tohoku Pharmaceutical University Hospital; Department of Neurology (O.T.), Sendai Medical Center; and Department of Neurology (A.T.), National Hospital Organization, Sendai Nishitaga Hospital, Sendai, Japan.
Abstract
OBJECTIVE: To determine whether 18F-THK5351 PET can be used to visualize tau deposits in brain lesions in live patients with corticobasal syndrome (CBS). METHODS: We evaluated the in vitro binding of 3H-THK5351 in postmortem brain tissues from a patient with corticobasal degeneration (CBD). In clinical PET studies, 18F-THK5351 retention in 5 patients with CBS was compared to that in 8 age-matched normal controls and 8 patients with Alzheimer disease (AD). RESULTS: 3H-THK5351 was able to bind to tau deposits in the postmortem brain with CBD. In clinical PET studies, the 5 patients with CBS showed significantly higher 18F-THK5351 retention in the frontal, parietal, and globus pallidus than the 8 age-matched normal controls and patients with AD. Higher 18F-THK5351 retention was observed contralaterally to the side associated with greater cortical dysfunction and parkinsonism. CONCLUSIONS: 18F-THK5351 PET demonstrated high tracer signal in sites susceptible to tau deposition in patients with CBS. 18F-THK5351 should be considered as a promising candidate radiotracer for the in vivo imaging of tau deposits in CBS.
OBJECTIVE: To determine whether 18F-THK5351 PET can be used to visualize tau deposits in brain lesions in live patients with corticobasal syndrome (CBS). METHODS: We evaluated the in vitro binding of 3H-THK5351 in postmortem brain tissues from a patient with corticobasal degeneration (CBD). In clinical PET studies, 18F-THK5351 retention in 5 patients with CBS was compared to that in 8 age-matched normal controls and 8 patients with Alzheimer disease (AD). RESULTS:3H-THK5351 was able to bind to tau deposits in the postmortem brain with CBD. In clinical PET studies, the 5 patients with CBS showed significantly higher 18F-THK5351 retention in the frontal, parietal, and globus pallidus than the 8 age-matched normal controls and patients with AD. Higher 18F-THK5351 retention was observed contralaterally to the side associated with greater cortical dysfunction and parkinsonism. CONCLUSIONS: 18F-THK5351 PET demonstrated high tracer signal in sites susceptible to tau deposition in patients with CBS. 18F-THK5351 should be considered as a promising candidate radiotracer for the in vivo imaging of tau deposits in CBS.
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