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.