Abstract
We sought to determine if upstream amyloid accumulation and downstream cognitive impairment have independent relationships with microglial activation and tau pathology. Fifty-eight older adults were stratified by amyloid and cognitive status based on (18)F-florbetaben PET, history, and neuropsychological testing. Of these, 57 had (11)C-PBR28 PET to measure microglial activation and 43 had (18)F-MK-6240 PET to measure tau pathology. Amyloid and cognitive status were associated with increased overall binding for both (11)C-PBR28 and (18)F-MK-6240 (p's < 0.01). While there was no interaction between amyloid and cognitive status in their association with (11)C-PBR28 binding (p = 0.6722), there was an interaction in their association with (18)F-MK-6240 binding (p = 0.0115). Binding of both radioligands was greater in amyloid-positive controls than in amyloid-negative controls; however, this difference was seen in neocortical regions for (11)C-PBR28 and only in medial temporal cortex for (18)F-MK-6240. We conclude that, in the absence of cognitive symptoms, amyloid deposition has a greater association with microglial activation than with tau pathology.