Aging is accompanied by declines in episodic memory and altered hippocampal function, each of which are exacerbated in response to the development of Alzheimer’s disease. Therefore, it is critical to identify factors which support resilience to such pathological aging. One proposed factor is redundancy, the existence of duplicate elements within a system that offers protection against failure. Redundancy is hypothesized to operate within the brain as a neuroprotective mechanism, though this hypothesis has not been tested in the context of neurodegenerative diseases. This dissertation presents initial evidence that hippocampal redundancy, quantified from resting-state functional brain networks, operates as a neuroprotective mechanism in aging.The role of hippocampal functional redundancy is examined in the context of clinical, cognitive, pathological, and experiential factors across three studies. The first study demonstrates that posterior hippocampal redundancy is lower in mild cognitive impairment, a precursor stage to Alzheimer’s disease, than in healthy aging, though redundancy does not differ between early and late stages of mild cognitive impairment. Further, posterior hippocampal redundancy is related to better memory performance. The second study expands upon these results, relating hippocampal redundancy to pathological markers of Alzheimer’s disease, showing that hippocampal redundancy mediates the relationship between hippocampal volume and memory performance. Additionally, the combination of low hippocampal redundancy, volume, and memory is associated with subsequent dementia conversion. The final study reveals that the positive mnemonic benefit of redundancy weakens throughout healthy older adulthood and is specific to posterior rather than anterior hippocampus. However, this study finds no evidence that redundancy is influenced by either education or physical activity, two prominent protective factors for healthy aging.Across these three studies, hippocampal redundancy, particularly in posterior regions, is shown to be associated with better clinical and cognitive outcomes. Future studies will benefit from longitudinal analysis of redundancy in relation to clinical progression and long-term measures of physical activity. Together, the results presented in this dissertation provide the initial evidence that hippocampal redundancy supports resilience to pathological aging.