COMPARISON BETWEEN SEMIQUANTITATIVE MEASURES AND READER CONCORDANCE OF AMYLOID LOAD BASED ON 18F-FLUTEMETAMOL VERSUS 11C-PIB IN COGNITIVELY INTACT OLDER ADULTS

Abstract

are associated with different patterns of regional brain atrophy is unresolved. We sought to determine whether the presence of b-amyloid (Ab) in the brain accelerates regional atrophy in a clinically-normal (CN) population in a region-specific manner, and to identify regions in which agerelated atrophy is significantly affected by early AD, measured by Ab PET.Methods: In 80 CN subjects with longitudinal volume measurements and Florbetapir PET, we used linear mixed effects models to determine the effects of Ab PET SUVR and age on longitudinal atrophy rates in 43 FreeSurfer regions of interest, while accounting for confounding variables including sex, ApoEe4 genotype, intracranial volume, white matter lesions, and tau levels. Results: Rates of atrophy in several temporal lobe regions were associated with Ab SUVR, with the strongest associations in entorhinal cortex and amygdala. When subjects were dichotomized into Ab+ and Absubgroups, high atrophy rates in distinct regions of the occipital, parietal, frontal, and cingulate cortices distinguished Ab+ versus Absubjects. Age was associated with atrophy rates in the insula, fusiform gyrus, and isthmus cingulate. There was a positive interaction between age and Ab status in predicting atrophy rates in pallidum, postcentral gyrus, and parahippocampal gyrus, indicating accelerated atrophy associated with the presence of Ab. In contrast, there was a negative interaction between age and Ab status in superior temporal gyrus, supramarginal gyrus, and lateral orbitofrontal gyrus indicating reduced atrophy associated with Ab. Conclusions: Brain Ab deposition largely accelerates atrophy of the same regions that show age-related atrophy, supporting a model in which age-related tau tangle accumulation in temporal lobe drives neurodegeneration and is accelerated by the presence of AD. The effects of age and Ab on brain atrophy rates may represent the combined effects of neurodegeneration, and compensatory processes responding to neurodegeneration.