TY - JOUR
T1 - Tau imaging with [18F]THK-5351 in progressive supranuclear palsy
AU - Ishiki, Aiko
AU - Harada, R.
AU - Okamura, Nobuyuki
AU - Tomita, N.
AU - Rowe, C. C.
AU - Villemagne, V. L.
AU - Yanai, K.
AU - Kudo, Yukitsuka
AU - Arai, Hiroyuki
AU - Furumoto, S.
AU - Tashiro, M.
AU - Furukawa, Katsutoshi
N1 - Funding Information:
The costs of publication of this article were defrayed in part by the payment of page charges. Therefore, and solely to indicate this fact, this article is hereby marked ?advertisement? in accordance with 18 United States Code (USC) section 1734. This study was supported by research funds from GE Healthcare, Sumitomo Electric Industries, Ltd Group CSR Foundation, Industrial Technology Research grant program of the NEDO in Japan (09E51025a), Health and Labor Sciences Research Grants from the Ministry of Health, Labor and Welfare of Japan, grant-in-aid for Scientific Research (B) (15H04900), grant-in-aid for Scientific Research on Innovative Areas (Brain Protein Aging and Dementia Control) (26117003), grant-in-aid for Young Scientists (B) (15K19767), and grant-in-aid for JSPS Fellows and Japan Advanced Molecular Imaging Program (J-AMP) of the Ministry of Education, Culture, Sports, Science and Technology (MEXT), Japan.
Publisher Copyright:
© 2016 EAN
PY - 2017/1/1
Y1 - 2017/1/1
N2 - Background and purpose: Visualization of pathogenic protein aggregates is crucial to elucidate pathomechanisms and to make an accurate diagnosis in many neurodegenerative conditions. Aggregates of the microtubule-binding protein, tau, are one of the most important pathogenic molecules in neurodegenerative disorders. Progressive supranuclear palsy (PSP) is characterized by the deposition of tau proteins in some specific area such as the basal ganglia and brainstem. We tried to detect tau lesions in the brains of living patients with PSP with a novel positron emission tomography (PET) tracer, [18F]THK-5351, which we have recently developed. Methods: Paraffin-embedded brain sections of the patients with PSP were used for autoradiography with [3H]THK-5351 and immunohistochemistry. Nine healthy controls, 13 patients with Alzheimer's disease and three patients with PSP participated in this PET study with [18F]THK-5351. To detect amyloid-β deposition, PET imaging with Pittsburgh compound B was also performed. Results: Autoradiography in the brain sections of patients with PSP demonstrated [3H]THK-5351 binding to tau deposits with a high selectivity. Although patients with PSP exhibited no remarkable [18F]THK-5351 retention in the temporal cortex, significantly higher tracer retention was observed in the globus pallidus and midbrain. In contrast, amyloid imaging with Pittsburgh compound B showed no remarkable accumulation in the cerebral cortex of PSP. Conclusions: We conclude that [18F]THK-5351 PET can potentially be used to detect the regional brain distribution of tau lesions in PSP, thereby facilitating the differential diagnosis of neurodegenerative disorders associated with tau protein.
AB - Background and purpose: Visualization of pathogenic protein aggregates is crucial to elucidate pathomechanisms and to make an accurate diagnosis in many neurodegenerative conditions. Aggregates of the microtubule-binding protein, tau, are one of the most important pathogenic molecules in neurodegenerative disorders. Progressive supranuclear palsy (PSP) is characterized by the deposition of tau proteins in some specific area such as the basal ganglia and brainstem. We tried to detect tau lesions in the brains of living patients with PSP with a novel positron emission tomography (PET) tracer, [18F]THK-5351, which we have recently developed. Methods: Paraffin-embedded brain sections of the patients with PSP were used for autoradiography with [3H]THK-5351 and immunohistochemistry. Nine healthy controls, 13 patients with Alzheimer's disease and three patients with PSP participated in this PET study with [18F]THK-5351. To detect amyloid-β deposition, PET imaging with Pittsburgh compound B was also performed. Results: Autoradiography in the brain sections of patients with PSP demonstrated [3H]THK-5351 binding to tau deposits with a high selectivity. Although patients with PSP exhibited no remarkable [18F]THK-5351 retention in the temporal cortex, significantly higher tracer retention was observed in the globus pallidus and midbrain. In contrast, amyloid imaging with Pittsburgh compound B showed no remarkable accumulation in the cerebral cortex of PSP. Conclusions: We conclude that [18F]THK-5351 PET can potentially be used to detect the regional brain distribution of tau lesions in PSP, thereby facilitating the differential diagnosis of neurodegenerative disorders associated with tau protein.
KW - positron emission tomography
KW - progressive supranuclear palsy
KW - tau
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U2 - 10.1111/ene.13164
DO - 10.1111/ene.13164
M3 - Article
C2 - 27797445
AN - SCOPUS:84996615294
VL - 24
SP - 130
EP - 136
JO - European Journal of Neurology
JF - European Journal of Neurology
SN - 1351-5101
IS - 1
ER -