O3‐02‐04: Does Neuroinflammation Predate Amyloid Formation in Subjects at Risk for Alzheimer’s Disease?

gitudinal). [F]FDG intensity was normalized to the pons. Baseline global cortical [F]Florbetapir and mean parietal [F]FDG SUVR, as well as 2yr annualized percent change (APC) in global [F]Florbetapir were extracted. Baseline and 2-year hippocampal volumes (HV) were estimated using Freesurfer v5.1. Step-wise linear models predicting cortical or MTL [F]AV-1451 SUVR with the following predictors were assessed: cortical [F]Florbetapir SUVR, annual percent change (APC) in cortical [F]Florbetapir SUVR, mean parietal [F]FDG SUVR, HV, APC in HV, diagnosis (control or MCI/AD), age, gender, and time between scans. Results:Mean cortical [F]AV-1451 uptake was predicted only by diagnosis and cross-sectional mean cortical [F]Florbetapir SUVR. However, MTL [F]AV-1451 uptake was predicted by both mean cross-sectional cortical [F]Florbetapir uptake and cross-sectional HV. Conclusions: Overall, [F]AV-1451 uptake (representative of tau deposition) was predicted by the extent of cortical amyloid deposition ([F]Florbetapir uptake) approximately three years prior. Hippocampal atrophy may interact with this process. [1] Risacher et al. (2015) Alzheimer’s & Dementia, (11): 1417.