Microglial activation, but not tau pathology, is independently associated with amyloid positivity and memory impairment

Zou, James Shiyang; Tao, Sha; Johnson, Aubrey S.; Tomljanovic, Zeljko; Polly, Krista; Klein, Julia; Razlighi, Qolamreza R.; Brickman, Adam M.; Lee, Seonjoo; Stern, Yaakov; Kreisl, William Charles

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 18F-florbetaben PET, history, and neuropsychological testing. Of these, 57 had 11C-PBR28 PET to measure microglial activation and 43 had 18F-MK-6240 PET to measure tau pathology. Amyloid and cognitive status were associated with increased overall binding for both 11C-PBR28 and 18F-MK-6240 (p’s < 0.01). While there was no interaction between amyloid and cognitive status in their association with 11C-PBR28 binding (p = 0.6722), there was an interaction in their association with 18F-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 11C-PBR28 and only in medial temporal cortex for 18F-MK-6240. We conclude that, in the absence of cognitive symptoms, amyloid deposition has a greater association with microglial activation than with tau pathology.


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May 4, 2021