Abstract
256
Background: We evaluated 18F-MK6240 to measure 3R/4R tau aggregate burden in the brain in Alzheimer’s disease (AD) and non-demented persons with past Traumatic Brain Injury (TBI).
Methods: We examined 128 participants: 70 healthy elderly controls (HC, 17 Aβ+), 8 mild cognitive impairment (MCI, 4 Aβ+), 10 Aβ+AD, 4 other dementia (OD, 1 Aβ+) and 36 TBI several decades earlier (5 Aβ+) due to single (MVA+VET) or repetitive (Sports) injuries. Mesial temporal and temporoparietal tracer binding was assessed using SUVR at 90-110 min post injection with cerebellar cortex as reference region. Cut-offs were set at two standard deviations above the mean binding in Aβ- HC.
Results: AD and MCI images showed high target to background with no off-target binding and limbic, neocortical or mixed distribution patterns. Nine of 10 Aβ+AD (90%), 2 of 4 Aβ+MCI (50%), 4 of17 Aβ+HC (24%) had high temporoparietal cortex 18F-MK6240 binding (Fig 1, top row). All Aβ+MCI and more Aβ+HC had high mesial temporal binding (Fig 1, bottom row). With the exception of one Aβ-HC and one Aβ+TBI, temporoparietal tracer retention in Aβ-HC, TBI and OD was low. Compared to Aβ-HC, significantly higher SUVR was observed in Aβ+HC in mesial temporal (0.95±0.17vs.1.27±0.42, p=0.0014), but not in temporoparietal cortex (1.01±0.14vs.1.17±0.39, p=0.32). Significantly higher SUVR was observed in Aβ+AD compared to Aβ-HC in mesial temporal (2.12±0.95 vs. 0.95±0.17, p<0.0001, Cohen’s d=1.7), and temporoparietal cortex 2.85±1.81 vs. 1.01±0.13, p<0.0001, Cohen’s d =1.4).
Conclusions: 18F-MK6240 PET discriminates well between AD and HC. In keeping with other recent biomarker studies, we found no evidence of increased AD pathology in persons with a remote history of traumatic brain injury.
