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Abstract

PURPOSE:
Tau accumulation is a core pathologic change in various neurodegenerative diseases including Alzheimer's disease and frontotemporal lobar degeneration-tau. Recently, tau positron emission tomography tracers such as [18F] AV-1451 and [18F] THK5351 have been developed to detect tau deposition in vivo. In the present study, we performed a head to head comparison of these two tracers in Alzheimer's disease and frontotemporal dementia cases and aimed to investigate which tracers are better suited to image tau in these disorders.

METHODS:
A cross-sectional study was conducted using a hospital-based sample at a tertiary referral center. We recruited eight participants (two Alzheimer's disease, four frontotemporal dementia and two normal controls) who underwent magnetic resonance image, amyloid positron emission tomography with [18F]-Florbetaben and tau positron emission tomography with both THK5351 and AV-1451. To measure regional AV1451 and THK5351 uptakes, we used the standardized uptake value ratios by dividing mean activity in target volume of interest by mean activity in the cerebellar hemispheric gray matter.

RESULTS:
Although THK5351 and AV-1451 uptakes were highly correlated, cortical uptake of AV-1451 was more striking in Alzheimer's disease, while cortical uptake of THK5351 was more prominent in frontotemporal dementia. THK5351 showed higher off-target binding than AV-1451 in the white matter, midbrain, thalamus, and basal ganglia.

CONCLUSIONS:
AV-1451 is more sensitive and specific to Alzheimer's disease type tau and shows lower off-target binding, while THK5351 may mirror non-specific neurodegeneration.

Author information

Jang YK1,2, Lyoo CH3, Park S1, Oh SJ4, Cho H3, Oh M4, Ryu YH5, Choi JY5, Rabinovici GD6,7, Kim HJ1,2, Moon SH8, Jang H1,2, Lee JS9, Jagust WJ7,10, Na DL1,2,11, Kim JS12, Seo SW13,14,15,16.

1 Department of Neurology, Samsung Medical Center, Sungkyunkwan University School of Medicine, 81 Irwon-ro, Kangnam-ku, Seoul, 06351, South Korea.
2 Neuroscience Center, Samsung Medical Center, Seoul, South Korea.
3 Department of Neurology, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, South Korea.
4 Department of Nuclear Medicine, Asan Medical Center, University of Ulsan College of Medicine, 88 Olympic-ro 43-gil, Songpa-gu, Seoul, 138-736, South Korea.
5 Department of Nuclear Medicine, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, South Korea.
6 Memory and Aging Center, University of California, San Francisco, San Francisco, CA, USA.
7 Helen Wills Neuroscience Institute, University of California, Berkeley, Berkeley, CA, USA.
8 Department of Nuclear Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, South Korea.
9 Department of Neurology, Kyung Hee University Hospital, Seoul, South Korea.
10 Center of Functional Imaging, Lawrence Berkeley National Laboratory, Berkeley, CA, USA.
11 Department of Health Sciences and Technology, SAIHST, Sungkyunkwan University, Seoul, South Korea.
12 Department of Nuclear Medicine, Asan Medical Center, University of Ulsan College of Medicine, 88 Olympic-ro 43-gil, Songpa-gu, Seoul, 138-736, South Korea. jaeskim@amc.seoul.kr.
13 Department of Neurology, Samsung Medical Center, Sungkyunkwan University School of Medicine, 81 Irwon-ro, Kangnam-ku, Seoul, 06351, South Korea. sangwonseo@empal.com.
14 Neuroscience Center, Samsung Medical Center, Seoul, South Korea. sangwonseo@empal.com.
15 Department of Health Sciences and Technology, SAIHST, Sungkyunkwan University, Seoul, South Korea. sangwonseo@empal.com.
16 Department of Clinical Research Design & Evaluation, SAIHST, Sungkyunkwan University, Seoul, South Korea. sangwonseo@empal.com.