RT Journal Article SR Electronic T1 To tau or to MAO-B? Most of the 18F-THK5351 signal is blocked by selegiline. JF Journal of Nuclear Medicine JO J Nucl Med FD Society of Nuclear Medicine SP 1644 OP 1644 VO 59 IS supplement 1 A1 Victor Villemagne A1 Vincent Dore A1 Nobuyuki Okamura A1 David Baxendale A1 Ryuichi Harada A1 Rachel Mulligan A1 Shozo Furumoto A1 Olivier Salvado A1 Kazuhiro Yanai A1 Colin Masters A1 Christopher Rowe YR 2018 UL http://jnm.snmjournals.org/content/59/supplement_1/1644.abstract AB 1644Background: : It has been reported that 18F-THK5351 binding in the brain of 5 mild cognitive impairment (MCI), two Alzheimer’s disease (AD), and 1 PSP subjects, was reduced by ~36% in the cortex and by ~50% in the basal ganglia 1-hr after a single 10-mg oral dose of the monoamine oxidase B (MAO-B) inhibitor selegiline. To explore if selegeline reduced 18F-THK5351 signal in the absence of tau, we investigated the degree of signal reduction after a 5-day regimen of oral selegiline not only in AD patients, but also in other dementias (OD) and age-matched healthy controls (HC). Methods: Ten participants (3 AD, 1 MCI, 4 HC and 2 OD), underwent a 18F-NAV4694 PET scan to ascertain amyloidosis, a baseline 18F-THK5351 scan, and a second 18F-THK5351 scan after a 5-day of a twice-daily 5-mg oral regimen of selegiline. Regional and global standardized uptake values (SUV), were generated for both NAV and THK studies. Results: After the 5-day regimen of selegiline, the regional SUV were significantly reduced by 82% in the basal ganglia, by 72% in the mesial temporal cortex and by 65% in neocortical regions (Figure 1). Despite being the area with the lowest 18F-THK5351 signal reduction, 55% of the cerebellar signal was reduced by selegiline. Interestingly, the same degree of regional signal reduction was observed in AD and HC participants. Conclusions: : Our results indicate that ~85% of the 18F-THK5351 signal in the basal ganglia and 60-75% of the 18F-THK5351 signal in cortical regions is reduced by selegiline. The fact that the same degree of signal reduction was observed in AD and HC participants, strongly suggests that the majority of 18F-THK5351 retention is not due to binding to tau deposits. These findings clearly indicate 18F-THK5351 should not be used to quantify tau deposits in the brain.