Tau neuropathology correlates with FDG-PET, but not AV-1451-PET, in progressive supranuclear palsy
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KeywordsPositron Emission Tomography Basal Ganglion Progressive Supranuclear Palsy Progressive Supranuclear Palsy Cerebellar Grey Matter
Radiotracers for tau have recently become available for positron emission tomography (PET) studies in neurodegenerative disorders. The currently most utilized tracer 18F-AV-1451 binds to paired helical filaments containing both 3R and 4R tau in Alzheimer’s disease (AD) in vitro [3, 4, 6]. Furthermore, 18F-AV-1451 can quantify AD-like tau pathology in MAPT R406W mutation carriers in vivo . In corticobasal degeneration, there is a clear binding to 4R tau pathology, but SUVRs are generally lower than in AD [2, 5].
In conclusion, the 18F-AV-1451 uptake in cerebral cortex and white matter does not reflect the tau pathology in PSP, possibly due to a less abundant tau pathology compared to AD and a lower affinity of AV-1451 for straight 4R filaments. In the basal ganglia and brain stem, where off-target binding is strong, it is unclear whether the increased 18F-AV-1451 reflects true tau pathology, even though the absence of specific autoradiographic binding in these structures argues against this notion. However, an increase in tau pathology is clearly associated with a decrease in 18F-FDG-PET.
We are grateful to the patient and his family for participating in the study. We also thank Drs. Tomas Björklund, Douglas Hägerström, Jonas Jögi, and Tomas Olsson. The study was supported by the European and the Swedish Research Councils. We are grateful to Avid radiopharmaceuticals for providing the precursor to AV-1451.
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