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