Publication Type Academic Article
Authors Zou J, Tao S, Johnson A, Tomljanovic Z, Polly K, Klein J, Razlighi Q, Brickman A, Lee S, Stern Y, Kreisl W
Journal Neurobiol Aging
Volume 85
Pagination 11-21
Date Published 09/29/2019
ISSN 1558-1497
Keywords Alzheimer Disease, Amyloid, Memory Disorders, Microglia
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 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.
DOI 10.1016/j.neurobiolaging.2019.09.019
PubMed ID 31698286
PubMed Central ID PMC6919274
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