Alzheimer’s disease (AD) is a devastating neurodegenerative disease characterized by the accumulation of amyloid-β plaques and neurofibrillary tangles in the brain, often leading to progressive cognitive decline and dementia. However, not everyone at risk of AD develops cognitive decline. Some individuals at high-risk do not show plaques and tangles, and other individuals who harbor plaques and tangles, consistent with an AD diagnosis, remain cognitive intact. These phenomena have been termed resistance – avoiding pathological accumulation – and resilience – coping with pathology to preserve cognition. Identifying the shared and distinct pathways and mechanisms involved in these neuroprotective mechanisms can lead to the development of different interventions to stop pathological progression (mimicking resistance mechanism) or prevent/stop cognitive impairment (mimicking resilience mechanism).