•Limbic and frontoparietal networks had a greater annual aβ accumulation in aging.•The annual aβ accumulation was negatively correlated with functional connectivity.•The aβ propagation over time was accelerated by the connectivity of functional hubs.•Functional brain organization compensates for aβ pathology and propagation in aging. The brain undergoes many changes at pathological and functional levels in healthy aging. This study employed a longitudinal and multimodal imaging dataset from the OASIS-3 study (n = 300) and explored possible relationships between amyloid beta (Aβ) accumulation and functional brain organization over time in healthy aging. We used positron emission tomography (PET) with Pittsburgh compound-B (PIB) to quantify the Aβ accumulation in the brain and resting-state functional MRI (rs-fMRI) to measure functional connectivity (FC) among brain regions. Each participant had at least 2 to 3 follow-up visits. A linear mixed-effect model was used to examine longitudinal changes of Aβ accumulation and FC throughout the whole brain. We found that the limbic and frontoparietal networks had a greater annual Aβ accumulation and a slower decline in FC in aging. Additionally, the amount of the Aβ deposition in the amygdala network at baseline slowed down the decline in its FC in aging. Furthermore, the functional connectivity of the limbic, default mode network (DMN), and frontoparietal networks accelerated the Aβ propagation across their functionally highly connected regions. The functional connectivity of the somatomotor and visual networks accelerated the Aβ propagation across the brain regions in the limbic, frontoparietal, and DMN networks. These findings suggested that the slower decline in the functional connectivity of the functional hubs may compensate for their greater Aβ accumulation in aging. The Aβ propagation from one brain region to the other may depend on their functional connectivity strength.