To understand how amyloidosis in Alzheimer’s Disease changes circuit properties affecting memory encoding and recall, we examined the relationship between neuronal activity, nearness to amyloid plaques, and spatial memory readout from hippocampal CA1 place cells. We performed two-photon calcium imaging in head-fixed 5xFAD mice navigating an air-lifted circular track. Neuronal hyperactivity in CA1 during non-running periods was higher in 5xFAD mice compared to wildtype littermates in both young (2-3 months) and old (6.5-10 months) groups. Moreover, neurons close to amyloid plaques (<20µm in old, <40µm in young) had elevated activity. Old 5xFAD mice ran faster than old wildtypes, but showed significantly impaired dynamic range of neuronal activity (5xFAD: 0.007±0.001 a.u./sec, n=2548 cells, 6 mice; wildtype: 0.067±0.003 a.u./sec, n=9666 cells, 6 mice). Compared to place cells in old wildtype mice, old 5xFAD place cells had lower activity, less spatial information and higher sparsity, indicating less place specificity. In young mice, place specificity was comparable between genotypes. However, young 5xFAD place cells had less spatial information and higher sparsity near plaques, suggesting that disrupted neural coding starts there. Finally, compared to wildtype mice, old 5xFAD mice required more laps around a familiar track for cells to exhibit place tuning, indicating impaired memory recall. Impaired memory encoding in a novel environment was similarly observed in 5xFAD mice in both age groups. Our study provides insight into the progression of spatial information coding deficits in 5xFAD mice and how these affect learning of new spatial memories versus recalling of old.