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Longitudinal florbetapir-PET and T1-weighted MRI data from 100 cognitively normal (CN) and mild cognitive impaired (MCI) participants both with considerable global A\u03b2 accumulation (\u201chigh A\u03b2 accumulators\u201d) were analyzed using a voxel-wise approach. Associations of APOE genotype and memory decline with A\u03b2 accumulation and GM atrophy were examined separately for each neuroimaging modality, controlling for baseline A\u03b2 levels and diagnosis. Alternatively, the effect of baseline diagnosis, while controlling for memory decline, was investigated. A multimodal analysis evaluated interactions between genotype, memory decline, and GM atrophy on A\u03b2 accumulation. High A\u03b2 accumulators displayed extensive A\u03b2 pathology predominantly in the medial orbito-frontal cortex, cingulate cortex, and precuneus, along with GM atrophy in temporal, occipital, orbito-frontal, and parietal areas. \u025b4 carriers with memory decline exhibited greater A\u03b2 accumulation and GM atrophy in selective regions compared to non-carriers with memory decline, while no genotype difference was observed in individuals without decline. No interaction effect was observed for MCI diagnosis. Regional associations between the two biomarkers were similarly dependent on genotype and memory decline. \u025b4 carriers exhibiting memory decline present an accelerated neurobiological pattern at predementia stages, supporting early \u025b4 carrier monitoring and interventions in this at-risk group. 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