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Eur J Nucl Med Mol Imaging. 2020 Feb;47(2):342-354. doi: 10.1007/s00259-019-04496-0. Epub 2019 Oct 14.

Head-to-head comparison of tau positron emission tomography tracers [18F]flortaucipir and [18F]RO948.

Author information

1
Clinical Memory Research Unit, Department of Clinical Sciences, Lund University, Malmö, Sweden. Ruben.Smith@med.lu.se.
2
Department of Neurology, Skåne University Hospital, Lund, Sweden. Ruben.Smith@med.lu.se.
3
Department of Neurology, Skåne University Hospital, SE-20502, Malmö, Sweden. Ruben.Smith@med.lu.se.
4
Clinical Memory Research Unit, Department of Clinical Sciences, Lund University, Malmö, Sweden.
5
Wallenberg Centre for Molecular and Translational Medicine and the Department of Psychiatry and Neurochemistry, University of Gothenburg, Gothenburg, Sweden.
6
Dementia Research Centre, Department of Neurodegenerative Disease, Queen Square Institute of Neurology, University College London, London, UK.
7
Department of Clinical Physiology and Nuclear Medicine, Skåne University Hospital, Lund, Sweden.
8
Department of Radiation Physics, Skåne University Hospital, Lund, Sweden.
9
Clinical Memory Research Unit, Department of Clinical Sciences, Lund University, Malmö, Sweden. Oskar.Hansson@med.lu.se.
10
Memory Clinic, Skåne University Hospital, SE-20502, Malmö, Sweden. Oskar.Hansson@med.lu.se.

Abstract

PURPOSE:

[18F]flortaucipir binds to paired helical filament tau and accurately identifies tau in Alzheimer's disease (AD). However, "off-target" binding interferes with the quantification of [18F]flortaucipir in several brain regions. Recently, other tau PET tracers have been developed. Here, we compare [18F]flortaucipir with the novel tau tracer [18F]RO948 head-to-head in vivo.

METHODS:

We included 18 participants with AD, three with amyloid-β-positive amnestic mild cognitive impairment, and four healthy controls. All underwent [18F]flortaucipir (80-100 min) and [18F]RO948 (70-90) PET scans within approximately 1 month. Four study participants underwent 0-100-min dynamic scanning. Standardized uptake value ratios (SUVRs) were created using an inferior cerebellar reference region.

RESULTS:

Neocortical tracer retention was highly comparable using both SUVR and distribution volume ratio-1 values obtained from dynamic scans. However, [18F]RO948 retention was significantly higher in the entorhinal cortex and lower in the basal ganglia, thalamus, and choroid plexus compared with [18F]flortaucipir. Increased off-target binding was observed with age for both tracers. Several cases exhibited strong [18F]RO948 retention in the skull/meninges. This extra-cerebral signal, however, did not affect diagnostic accuracy and remained relatively unchanged when re-examining a subsample after 1 year. Kinetic modeling showed an increase in [18F]flortaucipir SUVR over the scanning interval, compared with a plateau for [18F]RO948.

CONCLUSION:

[18F]RO948 and [18F]flortaucipir bound comparably in neocortical regions, but [18F]RO948 showed higher retention in the medial temporal lobe and lower intracerebral "off-target" binding. Time-dependent bias of SUVR estimates may prove less of a factor with [18F]RO948, compared with previous tau ligands.

KEYWORDS:

Alzheimer’s disease; Head-to-head; Neurodegeneration; PET; Tau

PMID:
31612245
DOI:
10.1007/s00259-019-04496-0

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