Please use this identifier to cite or link to this item: http://ahro.austin.org.au/austinjspui/handle/1/19131
Title: Tau imaging with [18 F]THK-5351 in progressive supranuclear palsy.
Authors: Ishiki, A;Harada, R;Okamura, N;Tomita, N;Rowe, Christopher C;Villemagne, Victor L;Yanai, K;Kudo, Y;Arai, H;Furumoto, S;Tashiro, M;Furukawa, K
Affiliation: Division of Community of Medicine, Faculty of Medicine, Tohoku Medical and Pharmaceutical University, Sendai, Japan
Division of Radiopharmaceutical Chemistry, Cyclotron and Radioisotope Center, Tohoku University, Sendai, Japan
Division of Cyclotron Nuclear Medicine, Cyclotron and Radioisotope Center, Tohoku University, Sendai, Japan
Division of Neuro-imaging, Institute of Development, Aging and Cancer, Tohoku University, Sendai, Japan
Department of Pharmacology, Tohoku University School of Medicine, Sendai, Japan
Division of Pharmacology, Faculty of Medicine, Tohoku Medical and Pharmaceutical University, Sendai, Japan
Department of Geriatrics and Gerontology, Institute of Development, Aging and Cancer, Tohoku University, Sendai, Japan
Centre for PET, Austin Health, Heidelberg, Victoria, Australia
The Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Melbourne, Victoria, Australia
Issue Date: Jan-2017
EDate: 2016-10-30
Citation: European journal of neurology 2017; 24(1): 130-136
Abstract: 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, [18 F]THK-5351, which we have recently developed. Paraffin-embedded brain sections of the patients with PSP were used for autoradiography with [3 H]THK-5351 and immunohistochemistry. Nine healthy controls, 13 patients with Alzheimer's disease and three patients with PSP participated in this PET study with [18 F]THK-5351. To detect amyloid-β deposition, PET imaging with Pittsburgh compound B was also performed. Autoradiography in the brain sections of patients with PSP demonstrated [3 H]THK-5351 binding to tau deposits with a high selectivity. Although patients with PSP exhibited no remarkable [18 F]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. We conclude that [18 F]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.
URI: http://ahro.austin.org.au/austinjspui/handle/1/19131
DOI: 10.1111/ene.13164
ORCID: 0000-0003-3910-2453
PubMed URL: 27797445
Type: Journal Article
Research Support, Non-U.S. Gov't
Subjects: positron emission tomography
progressive supranuclear palsy
tau
Appears in Collections:Journal articles

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