of the cerebral white matter, brainstem, and whole cerebellum (lon- gitudinal). [ 18 F]FDG intensity was normalized to the pons. Base- line global cortical [ 18 F]Florbetapir and mean parietal [ 18 F]FDG SUVR, as well as 2yr annualized percent change (APC) in global [ 18 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 [ 18 F]AV-1451 SUVR with the following predictors were assessed: cortical [ 18 F]Florbeta- pir SUVR, annual percent change (APC) in cortical [ 18 F]Florbeta- pir SUVR, mean parietal [ 18 F]FDG SUVR, HV, APC in HV, diagnosis (control or MCI/AD), age, gender, and time between scans. Results: Mean cortical [ 18 F]AV-1451 uptake was predicted only by diagnosis and cross-sectional mean cortical [ 18 F]Florbeta- pir SUVR. However, MTL [ 18 F]AV-1451 uptake was predicted by both mean cross-sectional cortical [ 18 F]Florbetapir uptake and cross-sectional HV. Conclusions: Overall, [ 18 F]AV-1451 uptake (representative of tau deposition) was predicted by the extent of cortical amyloid deposition ([ 18 F]Florbetapir uptake) approxi- mately three years prior. Hippocampal atrophy may interact with this process. [1] Risacher et al. (2015) Alzheimer’s & Dementia, (11): 1417. O3-02-03 REGIONAL ASSOCIATION BETWEEN CORTICAL VOLUMES AND IMAGING TAU PATHOLOGY USING 18 F-AV1451 AND 18 F-THK5351 Vincent Dore 1,2 , Pierrick Bourgeat 3 , Jurgen Fripp 3 , S Lance Macaulay 1 , Colin L. Masters 4 , David Ames 5,6 , Ralph N. Martins 7,8,9,10 , Olivier Salvado 3 , Christopher C. Rowe 2 , Victor L. Villemagne 4,11 and the. Australian Imaging, Biomarker and Lifestyle Flagship Study of Ageing (AIBL) Research Group, 1 CSIRO, Melbourne, Australia; 2 Austin Health, Melbourne, Australia; 3 CSIRO, Brisbane, Australia; 4 The Florey Institute of Neuroscience and Mental Health, Melbourne, Australia; 5 The University of Melbourne, Melbourne, Australia; 6 National Ageing Research Institute, Melbourne, Australia; 7 Cooperative Research Centre for Mental Health, Melbourne, Australia; 8 Sir James McCusker Alzheimer’s Disease Research Unit (Hollywood Private Hospital), Perth, Australia; 9 School of Psychiatry and Clinical Neurosciences, University of Western Australia, Perth, Australia; 10 Edith Cowan University, Perth, Australia; 11 Department of Molecular Imaging and Therapy, Centre for PET, Austin Health, Heidelberg, Australia. Contact e-mail: vincent.dore@csiro.au Background:Post mortem studies on Alzheimer’s disease (AD) have shown that the stereotypical pattern and density of tau deposition is strongly associated with cortical loss. The development of new PET ligands selective for tau now allows in vivo investigation of this as- sociation. Methods: Sixty-one participants underwent Tau imaging with 18 F-AV1451 (54-HC, 6-MCI, 1-AD) and forty-three others with 18 F-THK5351 (22-HC, 15-MCI, 6-AD). All participants received an MRI scan. Three tau masks corresponding to different Braak&Braak stages were constructed: Mesial-temporal (Me), Temporoparietal (Te) and Rest (R) of the neocortex. Tau and Ab PET scans were quantified using CapAIBL Ò . Tracer retention was measured in the three masks and normalized with three stan- dard reference regions: cerebellar cortex, pons and whole cere- bellum. A threshold was established for each mask and tau tracer. Cortical volumes were measured in the three masks using CurA- IBL Ò . Cortical volumes were adjusted for age and intra-cranial vol- ume. Results: From the three standard reference regions and for both tau tracers, the Pons SUVR normalization yielded the highest cor- relations with local cortical volumes in all three regions. THK-5351 and AV1451 SUVRPons estimated in Me were only associated with the cortical volumes of Me (r<-0.26,p¼0.04). THK-5351 SUVR- Pons, estimated in Te or R, and AV1451 SUVRPons, estimated in R, significantly correlated with the cortical volumes of all regions of interest (r<-0.43,p¼0.003) while AV1451 SUVRPons, esti- mated in Te, was significantly associated only with cortical vol- umes of Te and R (r<-0.27,p¼0.03). Categorically, studies with a “high” tau tracer retention in the Me or R regions had a significantly lower volumes (p<0.03) in the same investigated regions, while studies with a “high” tracer retention in Te had a significantly lower cortical volumes in all MeTeR regions (p<0.04). Conclusions:These preliminary results showed that tracer retention in the Me region was only associated with the cortical volumes of Me strengthening the hypothesis that tau deposition in this region is just part of the ageing process. However, tracer retention in the Te region was asso- ciated with cortical volumes in all estimated regions suggesting the Tau needs to spread in the Te region to observe more severe cortical damages. O3-02-04 DOES NEUROINFLAMMATION PREDATE AMYLOID FORMATION IN SUBJECTS AT RISK FOR ALZHEIMER’S DISEASE? Grazia Daniela Femminella, Melanie Dani, Zhen Fan, Valeria Calsolaro, Rebecca Atkinson, Adam Waldman, David J. Brooks, Paul Edison, Melanie Wood, Imperial College London, London, United Kingdom. Contact e-mail: paul.edison@imperial.ac.uk Background: Mild Cognitive Impairment (MCI) is a transitional stage between normal and Alzheimer’s disease (AD). AD sub- jects have significantly increased amyloid deposition and brain inflammation (microglial activity). Neuroinflammation has been proposed to be a link between amyloid deposition, neuronal dam- age and tangles formation. However, the in vivo relationship be- tween microglial activation and amyloid deposition has not been investigated simultaneously in a non-selected MCI population us- ing [11C]PBR28. Methods: 40 subjects (9 controls, 22 MCI, 9 AD) underwent [11C]PBR28 and [18F]Flutemetamol PET scans, as well as T1 and T2 magnetic resonance imaging and neuropsycho- metric evaluation. For [11C]PBR28, distribution volume (VT) and rate constants of the two tissue-compartmental model were calculated for each brain region. The amyloid load was estimated from 90–120’ target region:cerebellar [18F]Flutemetamol uptake ratios. [18F]Flutemetamol uptake was assessed by region of interest analysis. Results: 36% of MCI and 33% of AD subjects had increased glial activation, particularly evident in the frontal and occipital cortices in MCI and in posterior cingulate gyrus and temporal cortex in AD. MCI and AD showed significantly higher amyloid deposition in almost all the predefined cortical regions compared to controls; individually, 43.8% MCI and 80% AD were amyloid positive. Conclusions: This is the first time that increased [11C]PBR28 binding is reported in an MCI cohort which is in accordance with an early onset of neuroinflammatory changes in brain. This study suggests that microglial activation plays a significant role even in early stages of this disease, implying that individual stratification according to different path- ological substrates may be effective. O3-02-05 REGIONAL BRAIN AEROBIC GLYCOLYSIS ACROSS THE COGNITIVELY NORMAL ADULT LIFESPAN Andrei G. Vlassenko 1,2 , Manu S. Goyal 1,2 , Yi Su 2,3 , Tony J. Durbin 1,2 , Lars E. Couture 1 , Tammie L. S. Benzinger 2,3 , John C. Morris 2,4 , Marcus E. Raichle 2 , 1 Washington University School of Medicine, St. Louis, MO, USA; 2 Knight Alzheimer’s Disease Research Center, St. Louis, MO, USA; 3 Washington University in St. Louis School of Medicine, St. Louis, Podium Presentations: Tuesday, July 26, 2016 P283