Head to head comparison of [18F] AV-1451 and [18F] THK5351 for tau imaging in Alzheimer’s disease and frontotemporal dementia

• Published in: European journal of nuclear medicine and molecular imaging 2018-03, Vol.45 (3), p.432-442
• Main Authors: Jang, Young Kyoung, Lyoo, Chul Hyoung, Park, Seongbeom, Oh, Seung Jun, Cho, Hanna, Oh, Minyoung, Ryu, Young Hoon, Choi, Jae Yong, Rabinovici, Gil D., Kim, Hee Jin, Moon, Seung Hwan, Jang, Hyemin, Lee, Jin San, Jagust, William J., Na, Duk L., Kim, Jae Seung, Seo, Sang Won
• Format: Article
• Language: English
• Subjects: Alzheimer's disease; Amyloid; Basal ganglia; Binding; Cardiology; Cerebellum; Cortex; Degeneration; Dementia; Dementia disorders; Disease; Disease control; Emissions control; Frontotemporal dementia; Ganglia; Imaging; In vivo methods and tests; Magnetic resonance imaging; Medicine; Medicine & Public Health; Mesencephalon; Neurodegeneration; Neurodegenerative diseases; Neurological diseases; Nuclear Medicine; Oncology; Original Article; Orthopedics; Positron emission; Positron emission tomography; Radiology; Substantia alba; Substantia grisea; Tau protein; Thalamus; Tomography; Tracers
• ISSN: 1619-7070; 1619-7089
• DOI: 10.1007/s00259-017-3876-0

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 [ 18 F] AV-1451 and [ 18 F] 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 [ 18 F]-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.