[P4–529]: AMYLOID LOAD: A NOVEL BIOMARKER WITH INCREASED SENSITIVITY FOR β‐AMYLOID

and with respect to a common temporal frame, to consistently account for spatial and temporal misalignement of the images from different modalities and time points; iii) analysed at the voxel-level in order to identify the multimodal pattern of neurodegeneration spanning the whole disease time course. Results:The estimated disease progression spans roughly 20 years. It is characterised by initial amyloid deposition in parietal and temporal regions (Figure 1) reaching a plateau 10 years after the model baseline (year 0). Posterior hypometabolism appears at year 5 and further evolves to parietal and temporal regions (Figure 2). Hippocampal and temporal atrophy appear later, roughly 10 years after the initial amyloid deposition (Figure 3). At the latest stages the model shows the stereotypical pattern of posterior/temporal and parietal hypometabolim and amyloid deposition, along with the atrophy pattern spread across temporal cortical/subcortical areas. Conclusions: This work develops for the first time an in-silico high-resolution image-based computational model of the multimodal relationship between brain atrophy, hypometabolism and amyloid deposition in AD. The model highlights spatio-temporal neurodegeneration patterns compatible with previous imaging findings and with classical hypothetical models of AD progression. The model provides an unprecedented reference for the quantification of the severity of the disease in clinical trials of disease modifying drugs. P4-529 AMYLOID LOAD: A NOVEL BIOMARKER WITH INCREASED SENSITIVITY FOR b-AMYLOID Alex Whittington, David J. Sharp, Roger N. Gunn, Imperial College London, London, United Kingdom; IMANOVA Ltd., London, United Kingdom. Contact e-mail: Roger.Gunn@ Imanova.co.uk